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1
Hadjivasiliou, Zena, Andrew Pomiankowski, Robert M. Seymour, and Nick Lane. "Selection for mitonuclear co-adaptation could favour the evolution of two sexes." Proceedings of the Royal Society B: Biological Sciences 279, no. 1734 (December 7, 2011): 1865–72. http://dx.doi.org/10.1098/rspb.2011.1871.
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Mitochondria are descended from free-living bacteria that were engulfed by another cell between one and a half to two billion years ago. A redistribution of DNA led to most genetic information being lost or transferred to a large central genome in the nucleus, leaving a residual genome in each mitochondrion. Oxidative phosphorylation, the most critical function of mitochondria, depends on the functional compatibility of proteins encoded by both the nucleus and mitochondria. We investigate whether selection for adaptation between the nuclear and mitochondrial genomes (mitonuclear co-adaptation) could, in principle, have promoted uniparental inheritance of mitochondria and thereby the evolution of two mating types or sexes. Using a mathematical model, we explore the importance of the radical differences in ploidy levels, sexual and asexual modes of inheritance, and mutation rates of the nucleus and mitochondria. We show that the major features of mitochondrial inheritance, notably uniparental inheritance and bottlenecking, enhance the co-adaptation of mitochondrial and nuclear genes and therefore improve fitness. We conclude that, under a wide range of conditions, selection for mitonuclear co-adaptation favours the evolution of two distinct mating types or sexes in sexual species.
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Levitskii, Baleva, Chicherin, Krasheninnikov, and Kamenski. "S. cerevisiae Strain Lacking Mitochondrial IF3 Shows Increased Levels of Tma19p during Adaptation to Respiratory Growth." Cells 8, no. 7 (June 26, 2019): 645. http://dx.doi.org/10.3390/cells8070645.
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After billions of years of evolution, mitochondrion retains its own genome, which gets expressed in mitochondrial matrix. Mitochondrial translation machinery rather differs from modern bacterial and eukaryotic cytosolic systems. Any disturbance in mitochondrial translation drastically impairs mitochondrial function. In budding yeast Saccharomyces cerevisiae, deletion of the gene coding for mitochondrial translation initiation factor 3 - AIM23, leads to an imbalance in mitochondrial protein synthesis and significantly delays growth after shifting from fermentable to non-fermentable carbon sources. Molecular mechanism underlying this adaptation to respiratory growth was unknown. Here, we demonstrate that slow adaptation from glycolysis to respiration in the absence of Aim23p is accompanied by a gradual increase of cytochrome c oxidase activity and by increased levels of Tma19p protein, which protects mitochondria from oxidative stress.
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Braun, Ralf J., and Benedikt Westermann. "Mitochondrial dynamics in yeast cell death and aging." Biochemical Society Transactions 39, no. 5 (September 21, 2011): 1520–26. http://dx.doi.org/10.1042/bst0391520.
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Mitochondria play crucial roles in programmed cell death and aging. Different stimuli activate distinct mitochondrion-dependent cell death pathways, and aging is associated with a progressive increase in mitochondrial damage, culminating in oxidative stress and cellular dysfunction. Mitochondria are highly dynamic organelles that constantly fuse and divide, forming either interconnected mitochondrial networks or separated fragmented mitochondria. These processes are believed to provide a mitochondrial quality control system and enable an effective adaptation of the mitochondrial compartment to the metabolic needs of the cell. The baker's yeast, Saccharomyces cerevisiae, is an established model for programmed cell death and aging research. The present review summarizes how mitochondrial morphology is altered on induction of cell death or on aging and how this correlates with the induction of different cell death pathways in yeast. We highlight the roles of the components of the mitochondrial fusion and fission machinery that affect and regulate cell death and aging.
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Ballantyne, J. S., and M. E. Chamberlin. "Adaptation and evolution of mitochondria: osmotic and ionic considerations." Canadian Journal of Zoology 66, no. 5 (May 1, 1988): 1028–35. http://dx.doi.org/10.1139/z88-152.
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Mitochondrial evolution has been examined on the basis of properties of mitochondria from representatives of key adaptive stages. The major step in the evolution of mitochondria was the transfer of mitochondrial genes to the nucleus to take advantage of recombination during meiosis. The ensuing increase in variability facilitated adaptation to environmental stress. The role of environmental factors such as atmospheric oxygen levels in the evolution of mitochondria is discussed on the basis of evidence obtained from mitochondria of living representatives of important groups and the fossil record. Rate enhancement has been a central theme in the evolution of animal mitochondria. Optimization of mitochondrial oxidation rates occurred through adjustments in intracellular solute systems. This took place in several stages, including (i) a reduction of intracellular inorganic ion levels by substitution of a variety of compatible solutes, (ii) a counteracting solute system (urea and methylamines), and (iii) osmoregulation.
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Johnston, I. A., H. Guderley, C. E. Franklin, T. Crockford, and C. Kamunde. "ARE MITOCHONDRIA SUBJECT TO EVOLUTIONARY TEMPERATURE ADAPTATION?" Journal of Experimental Biology 195, no. 1 (October 1, 1994): 293–306. http://dx.doi.org/10.1242/jeb.195.1.293.
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Thermal tolerance and the respiratory properties of isolated red muscle mitochondria were investigated in Oreochromis alcalicus grahami from the alkaline hot-springs, Lake Magadi, Kenya. Populations of O. a. grahami were resident in pools at 42.8 °C and migrated into water reaching temperatures of 44.8 °C for short periods. The maximum respiration rates of mitochondria with pyruvate as substrate were 217 and 284 natom O mg-1 mitochondrial protein min-1 at 37 °C and 42 °C, respectively (Q10=1.71). Fatty acyl carnitines (chain lengths C8, C12 and C16), malate and glutamate were oxidised at 70­80 % of the rate for pyruvate. In order to assess evolutionary temperature adaptation of maximum mitochondrial oxidative capacities, the rates of pyruvate and palmitoyl carnitine utilisation in red muscle mitochondria were measured from species living at other temperatures: Notothenia coriiceps from Antarctica (-1.5 to +1 °C); summer-caught Myoxocephalus scorpius from the North Sea (10­15 °C); and Oreochromis andersoni from African lakes and rivers (22­30 °C). State 3 respiration rates had Q10 values in the range 1.8­2.7. At the lower lethal temperature of O. andersoni (12.5 °C), isolated mitochondria utilised pyruvate at a similar rate to mitochondria from N. coriiceps at 2.5 °C (30 natom O mg-1 mitochondrial protein min-1). Rates of pyruvate oxidation by mitochondria from M. scorpius and N. coriiceps were similar and were higher at a given temperature than for O. andersoni. At their normal body temperature (-1.2 °C), mitochondria from the Antarctic fish oxidised pyruvate at 5.5 % and palmitoyl-dl-carnitine at 8.8 % of the rates of mitochondria from the hot-spring species at 42 °C. The results indicate only modest evolutionary adjustments in the maximal rates of mitochondrial respiration in fish living at different temperatures.
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Johnson, Gyasi, Damien Roussel, Jean-François Dumas, Olivier Douay, Yves Malthièry, Gilles Simard, and Patrick Ritz. "Influence of intensity of food restriction on skeletal muscle mitochondrial energy metabolism in rats." American Journal of Physiology-Endocrinology and Metabolism 291, no. 3 (September 2006): E460—E467. http://dx.doi.org/10.1152/ajpendo.00258.2005.
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Variable durations of food restriction (FR; lasting weeks to years) and variable FR intensities are applied to animals in life span-prolonging studies. A reduction in mitochondrial proton leak is suggested as a putative mechanism linking such diet interventions and aging retardation. Early mechanisms of mitochondrial metabolic adaptation induced by FR remain unclear. We investigated the influence of different degrees of FR over 3 days on mitochondrial proton leak and mitochondrial energy metabolism in rat hindlimb skeletal muscle. Animals underwent 25, 50, and 75% and total FR compared with control rats. Proton leak kinetics and mitochondrial functions were investigated in two mitochondrial subpopulations, intermyofibrillar (IMF) and subsarcolemmal (SSM) mitochondria. Regardless of the degree of restriction, skeletal muscle mass was not affected by 3 days of FR. Mitochondrial basal proton conductance was significantly decreased in 50% restricted rats in both mitochondrial subpopulations (46 and 40% for IMF and SSM, respectively) but was unaffected in other groups compared with controls. State 3 and uncoupled state 3 respiration rates were decreased in SSM mitochondria only for 50% restricted rats when pyruvate + malate was used as substrate (−34.5 and −38.9% compared with controls, P < 0.05). IMF mitochondria respiratory rates remained unchanged. Three days of FR, particularly at 50% FR, were sufficient to lower mitochondria energetic metabolism in both mitochondrial populations. Our study highlights an early step in mitochondrial adaptation to FR and the influence of the severity of restriction on this adaptation. This step may be involved in an aging-retardation process.
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Barreto, Pedro, Alessandra Koltun, Juliana Nonato, Juliana Yassitepe, Ivan de Godoy Maia, and Paulo Arruda. "Metabolism and Signaling of Plant Mitochondria in Adaptation to Environmental Stresses." International Journal of Molecular Sciences 23, no. 19 (September 23, 2022): 11176. http://dx.doi.org/10.3390/ijms231911176.
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The interaction of mitochondria with cellular components evolved differently in plants and mammals; in plants, the organelle contains proteins such as ALTERNATIVE OXIDASES (AOXs), which, in conjunction with internal and external ALTERNATIVE NAD(P)H DEHYDROGENASES, allow canonical oxidative phosphorylation (OXPHOS) to be bypassed. Plant mitochondria also contain UNCOUPLING PROTEINS (UCPs) that bypass OXPHOS. Recent work revealed that OXPHOS bypass performed by AOXs and UCPs is linked with new mechanisms of mitochondrial retrograde signaling. AOX is functionally associated with the NO APICAL MERISTEM transcription factors, which mediate mitochondrial retrograde signaling, while UCP1 can regulate the plant oxygen-sensing mechanism via the PRT6 N-Degron. Here, we discuss the crosstalk or the independent action of AOXs and UCPs on mitochondrial retrograde signaling associated with abiotic stress responses. We also discuss how mitochondrial function and retrograde signaling mechanisms affect chloroplast function. Additionally, we discuss how mitochondrial inner membrane transporters can mediate mitochondrial communication with other organelles. Lastly, we review how mitochondrial metabolism can be used to improve crop resilience to environmental stresses. In this respect, we particularly focus on the contribution of Brazilian research groups to advances in the topic of mitochondrial metabolism and signaling.
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Tobler, M., N. Barts, and R. Greenway. "Mitochondria and the Origin of Species: Bridging Genetic and Ecological Perspectives on Speciation Processes." Integrative and Comparative Biology 59, no. 4 (April 20, 2019): 900–911. http://dx.doi.org/10.1093/icb/icz025.
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Abstract Mitochondria have been known to be involved in speciation through the generation of Dobzhansky–Muller incompatibilities, where functionally neutral co-evolution between mitochondrial and nuclear genomes can cause dysfunction when alleles are recombined in hybrids. We propose that adaptive mitochondrial divergence between populations can not only produce intrinsic (Dobzhansky–Muller) incompatibilities, but could also contribute to reproductive isolation through natural and sexual selection against migrants, post-mating prezygotic isolation, as well as by causing extrinsic reductions in hybrid fitness. We describe how these reproductive isolating barriers can potentially arise through adaptive divergence of mitochondrial function in the absence of mito-nuclear coevolution, a departure from more established views. While a role for mitochondria in the speciation process appears promising, we also highlight critical gaps of knowledge: (1) many systems with a potential for mitochondrially-mediated reproductive isolation lack crucial evidence directly linking reproductive isolation and mitochondrial function; (2) it often remains to be seen if mitochondrial barriers are a driver or a consequence of reproductive isolation; (3) the presence of substantial gene flow in the presence of mito-nuclear incompatibilities raises questions whether such incompatibilities are strong enough to drive speciation to completion; and (4) it remains to be tested how mitochondrial effects on reproductive isolation compare when multiple mechanisms of reproductive isolation coincide. We hope this perspective and the proposed research plans help to inform future studies of mitochondrial adaptation in a manner that links genotypic changes to phenotypic adaptations, fitness, and reproductive isolation in natural systems, helping to clarify the importance of mitochondria in the formation and maintenance of biological diversity.
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Assayag, Miri, Ann Saada, Gary Gerstenblith, Haifa Canaana, Rivka Shlomai, and Michal Horowitz. "Mitochondrial performance in heat acclimation—a lesson from ischemia/reperfusion and calcium overload insults in the heart." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 303, no. 8 (October 15, 2012): R870—R881. http://dx.doi.org/10.1152/ajpregu.00155.2012.
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Long-term heat acclimation (LTHA; 30 days, 34°C) causes phenotypic adaptations that render protection against ischemic/reperfusion insult (I/R, 30 min global ischemia and 40 min reperfusion) via heat acclimation-mediated cross-tolerance (HACT) mechanisms. Short-term acclimation (STHA, 2 days, 34°C), in contrast, is characterized by cellular perturbations, leading to increased susceptibility to insults. Here, we tested the hypothesis that enhanced mitochondrial respiratory function is part of the acclimatory repertoire and that the 30-day regimen is required for protection via HACT. We subjected isolated hearts and mitochondria from controls (C), STHA, or LTHA rats to I/R, hypoxia/reoxygenation, or Ca2+ overload insults. Mitochondrial function was assessed by measuring O2 consumption, membrane potential (ΔΨm), mitochondrial Ca2+ ([Ca2+]m), ATP production, respiratory chain complex activities, and molecular markers of mitochondrial biogenesis. Our results, combining physiological and biochemical parameters, confirmed that mitochondria from LTHA rats subjected to insults, in contrast to C, preserve respiratory functions (e.g., upon I/R, C mitochondria fueled by glutamate-malate, demonstrated decreases of 81%, 13%, 25%, and 50% in O2/P ratio, ATP production, ΔΨm, and complex I activity, respectively, whereas the corresponding LTHA parameters remained unchanged). STHA mitochondria maintained ΔΨm but did not preserve ATP production. LTHA [Ca2+]m was significantly higher than that of C and STHA and was not affected by the hypoxia/reoxygenation protocol compared with C. Enhanced mitochondrial biogenesis markers, switched-on during STHA coincidentally with enhanced membrane integrity (ΔΨm), were insufficient to confer intact respiratory function upon insult. LTHA was required for respiratory complex I adaptation and HACT. Stabilized higher basal [Ca2+]m and attenuated Ca2+ overload are likely connected to this adaptation.
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Zhao, Ruzhou, Yixin Xu, Xiaobo Wang, Xiang Zhou, Yanqi Liu, Shuai Jiang, Lin Zhang, and Zhibin Yu. "Withaferin A Enhances Mitochondrial Biogenesis and BNIP3-Mediated Mitophagy to Promote Rapid Adaptation to Extreme Hypoxia." Cells 12, no. 1 (December 25, 2022): 85. http://dx.doi.org/10.3390/cells12010085.
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Rapid adaptation to extreme hypoxia is a challenging problem, and there is no effective scheme to achieve rapid adaptation to extreme hypoxia. In this study, we found that withaferin A (WA) can significantly reduce myocardial damage, maintain cardiac function, and improve survival in rats in extremely hypoxic environments. Mechanistically, WA protects against extreme hypoxia by affecting BCL2-interacting protein 3 (BNIP3)-mediated mitophagy and the peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α)-mediated mitochondrial biogenesis pathway among mitochondrial quality control mechanisms. On the one hand, enhanced mitophagy eliminates hypoxia-damaged mitochondria and prevents the induction of apoptosis; on the other hand, enhanced mitochondrial biogenesis can supplement functional mitochondria and maintain mitochondrial respiration to ensure mitochondrial ATP production under acute extreme hypoxia. Our study shows that WA can be used as an effective drug to improve tolerance to extreme hypoxia.
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Scheede-Bergdahl, Celena, and Andreas Bergdahl. "Adaptation of mitochondrial expression and ATP production in dedifferentiating vascular smooth muscle cells." Canadian Journal of Physiology and Pharmacology 95, no. 12 (December 2017): 1473–79. http://dx.doi.org/10.1139/cjpp-2017-0227.
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Atherosclerosis is one of the leading causes of morbidity and mortality in the Western world. Although the clinical manifestations of this disease are well documented, the etiology and progression remain to be fully understood. Recently, the mitochondria have been implicated in important cellular processes involved in development of atherosclerosis. Despite the link between mitochondria and atherosclerosis, early-phase mechanisms of the disease have yet to be elucidated. The aim of this project was to explore the role of mitochondria in vascular smooth muscle (VSMC) dedifferentiation. A murine in vitro model, involving organ culture of aortic tissue in serum-free media, was used. Mitochondrial function was measured by high-resolution respirometry. Proteins associated with the VSMC phenotype switch, as well as mitochondrial density, were assessed by immunoblotting. The findings show that intrinsic mitochondrial Complex I activity is significantly upregulated during VSMC dedifferentiation. Diminished coupling between phosphorylation and oxidation was also found, indicating a greater ADP:ATP ratio. This data suggests increased leak in the electron transport chain and altered mitochondrial function specifically at Complex I. This project provides important information regarding the role of mitochondria in the early atherosclerotic process and that detectable changes in mitochondrial function and expression are related to VSMC dedifferentiation.
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Li, Busu, Huan Wang, Xianghui Zeng, Shufang Liu, and Zhimeng Zhuang. "Mitochondrial Homeostasis Regulating Mitochondrial Number and Morphology Is a Distinguishing Feature of Skeletal Muscle Fiber Types in Marine Teleosts." International Journal of Molecular Sciences 25, no. 3 (January 26, 2024): 1512. http://dx.doi.org/10.3390/ijms25031512.
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Fishes’ skeletal muscles are crucial for swimming and are differentiated into slow-twitch muscles (SM) and fast-twitch muscles (FM) based on physiological and metabolic properties. Consequently, mitochondrial characteristics (number and morphology) adapt to each fiber type’s specific functional needs. However, the mechanisms governing mitochondrial adaptation to the specific bioenergetic requirements of each fiber type in teleosts remain unclear. To address this knowledge gap, we investigated the mitochondrial differences and mitochondrial homeostasis status (including biogenesis, autophagy, fission, and fusion) between SM and FM in teleosts using Takifugu rubripes as a representative model. Our findings reveal that SM mitochondria are more numerous and larger compared to FM. To adapt to the increased mitochondrial number and size, SM exhibit elevated mitochondrial biogenesis and dynamics (fission/fusion), yet show no differences in mitochondrial autophagy. Our study provides insights into the adaptive mechanisms shaping mitochondrial characteristics in teleost muscles. The abundance and elongation of mitochondria in SM are maintained through elevated mitochondrial biogenesis, fusion, and fission, suggesting an adaptive response to fulfill the bioenergetic demands of SM that rely extensively on OXPHOS in teleosts. Our findings enhance our understanding of mitochondrial adaptations in diverse muscle types among teleosts and shed light on the evolutionary strategies of bioenergetics in fishes.
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MacInnis, Martin J., Maria E. Haikalis, Brian J. Martin, Lauren E. Skelly, Jenna B. Gillen, Mark A. Tarnopolsky, and Martin J. Gibala. "Mitochondrial Adaptation To Training." Medicine & Science in Sports & Exercise 48 (May 2016): 747. http://dx.doi.org/10.1249/01.mss.0000487242.86433.6c.
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Havird, Justin C., Alisha A. Shah, and Adam J. Chicco. "Powerhouses in the cold: mitochondrial function during thermal acclimation in montane mayflies." Philosophical Transactions of the Royal Society B: Biological Sciences 375, no. 1790 (December 2, 2019): 20190181. http://dx.doi.org/10.1098/rstb.2019.0181.
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Mitochondria provide the vast majority of cellular energy available to eukaryotes. Therefore, adjustments in mitochondrial function through genetic changes in mitochondrial or nuclear-encoded genes might underlie environmental adaptation. Environmentally induced plasticity in mitochondrial function is also common, especially in response to thermal acclimation in aquatic systems. Here, we examined mitochondrial function in mayfly larvae ( Baetis and Drunella spp.) from high and low elevation mountain streams during thermal acclimation to ecologically relevant temperatures. A multi-substrate titration protocol was used to evaluate different respiratory states in isolated mitochondria, along with cytochrome oxidase and citrate synthase activities. In general, maximal mitochondrial respiratory capacity and oxidative phosphorylation coupling efficiency decreased during acclimation to higher temperatures, suggesting montane insects may be especially vulnerable to rapid climate change. Consistent with predictions of the climate variability hypothesis, mitochondria from Baetis collected at a low elevation site with highly variable daily and seasonal temperatures exhibited greater thermal tolerance than Baetis from a high elevation site with comparatively stable temperatures. However, mitochondrial phenotypes were more resilient than whole-organism phenotypes in the face of thermal stress. These results highlight the complex relationships between mitochondrial and organismal genotypes, phenotypes and environmental adaptation. This article is part of the theme issue ‘Linking the mitochondrial genotype to phenotype: a complex endeavour’.
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Valsecchi, Federica, Lavoisier S. Ramos-Espiritu, Jochen Buck, Lonny R. Levin, and Giovanni Manfredi. "cAMP and Mitochondria." Physiology 28, no. 3 (May 2013): 199–209. http://dx.doi.org/10.1152/physiol.00004.2013.
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Phosphorylation of mitochondrial proteins has emerged as a major regulatory mechanism for metabolic adaptation. cAMP signaling and PKA phosphorylation of mitochondrial proteins have just started to be investigated, and the presence of cAMP-generating enzymes and PKA inside mitochondria is still controversial. Here, we discuss the role of cAMP in regulating mitochondrial bioenergetics through protein phosphorylation and the evidence for soluble adenylyl cyclase as the source of cAMP inside mitochondria.
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Ferro, M., G. Rodrigues, and R. De Souza. "The role of mitochondria in physical activity and its adaptation on aging." Journal of Morphological Sciences 32, no. 04 (October 2015): 257–63. http://dx.doi.org/10.4322/jms.079114.
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Abstract Introduction: The mitochondria are essential in numerous physiological processes, including energy production, redox potential, modulation of calcium and several metabolic pathways. When the number or mitochondrial activity is insufficient, the human body quickly goes into fatigue due to ATP deficiency. Methods: The principal data base were used: PubMed, Medline, Scielo and Lilacs. Keywords used were: mitochondrial biogenesis, aging, organic acids, enzyme changes and respiratory chain. Groups considered: young and aged. Types of training: aerobic and anaerobic. Papers dealing with pathogies were not considered. The oxidative capacity of muscle tissue and the preservation of mitochondria depends on the mitochondrial biogenesis that occurs through the transcription factor proliferator-activator receptor-γ coactivatorlα (PGC-1α). The oxidative process and the progressive change in the biogenesis of mitochondria have direct influence on the aging of muscle tissue. The regulation of the biogenesis occurs through the PGC-1α combined with nuclear respiratory factor 1 (NRF1). Abnormalities in mitochondria and mutagenesis in mitochondrial DNA (mtDNA) are tied to multi-system degeneration, as well as intolerance to stress, and decreased energy in aging in humans, rats and monkeys. The mitochondrial functions are dramatically altered in heart disease, demonstrating a decrease in expression of PGC-1α, which plays a key role in the coordination of energy metabolism. This process can be reversed by the PGC-1α itself. The identification of compounds capable of activating the transcription of PGC-1α could be part of future therapies to reverse pathologies associated with the decline of this organelle. Morpho-physiological and biochemical changes of these organelles directly reflect the physiological performance of all body tissues. Conclusion: evidence demonstrated that physical activity, both in young and aged is a major ally in mitochondrial biogenesis by activating the transcription of PGC - 1α and that future nutritional interventions may be of great aid in the health and performance of mitochondria. However, further studies are needed in order to understand and clarify this operation, since currently these mechanisms are only partially known.
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Valcarce, C., J. M. Izquierdo, M. Chamorro, and J. M. Cuezva. "Mammalian adaptation to extrauterine environment: mitochondrial functional impairment caused by prematurity." Biochemical Journal 303, no. 3 (November 1, 1994): 855–62. http://dx.doi.org/10.1042/bj3030855.
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In this paper we report that, compared with term rat neonates, both mitochondrial content and function are diminished in liver of preterm neonates (delivered 24 h before full term) compromising cellular energy provision in the postnatal period. In addition, there is a parallel reduction in the content of mRNAs encoding mitochondrial proteins in preterm rats. Also, efficient oxidative phosphorylation is not attained in these pups until 3 h after birth. Although isolated liver mitochondria from preterm neonates show a two-fold increase in F1-ATPase beta-subunit and cytochrome c oxidase activity 1 h after birth, the abnormal coupling efficiency between respiration and oxidative phosphorylation (ADP/O ratio) is due to maintenance of high H(+)-leakage values in the inner mitochondrial membrane. Postnatal reduction of the H+ leak occurs concomitantly with an increase in intra-mitochondrial adenine nucleotide concentration. Accumulation of adenine nucleotides in preterm and term liver mitochondria parallels the postnatal increase in total liver adenine nucleotides. Delayed postnatal induction of adenine biosynthesis most likely accounts for the lower adenine nucleotide pool in the liver of preterm neonates. The delayed postnatal accumulation of adenine nucleotides in mitochondria is thus responsible for the impairment in oxidative phosphorylation displayed by organelles of the preterm liver.
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Ghiselli, Fabrizio, and Liliana Milani. "Linking the mitochondrial genotype to phenotype: a complex endeavour." Philosophical Transactions of the Royal Society B: Biological Sciences 375, no. 1790 (December 2, 2019): 20190169. http://dx.doi.org/10.1098/rstb.2019.0169.
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Finding causal links between genotype and phenotype is a major issue in biology, even more in mitochondrial biology. First of all, mitochondria form complex networks, undergoing fission and fusion and we do not know how such dynamics influence the distribution of mtDNA variants across the mitochondrial network and how they affect the phenotype. Second, the non-Mendelian inheritance of mitochondrial genes can have sex-specific effects and the mechanism of mitochondrial inheritance is still poorly understood, so it is not clear how selection and/or drift act on mtDNA genetic variation in each generation. Third, we still do not know how mtDNA expression is regulated; there is growing evidence for a convoluted mechanism that includes RNA editing, mRNA stability/turnover, post-transcriptional and post-translational modifications. Fourth, mitochondrial activity differs across species as a result of several interacting processes such as drift, adaptation, genotype-by-environment interactions, mitonuclear coevolution and epistasis. This issue will cover several aspects of mitochondrial biology along the path from genotype to phenotype, and it is subdivided into four sections focusing on mitochondrial genetic variation, on the relationship among mitochondria, germ line and sex, on the role of mitochondria in adaptation and phenotypic plasticity, and on some future perspectives in mitochondrial research. This article is part of the theme issue ‘Linking the mitochondrial genotype to phenotype: a complex endeavour’.
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Vara-Perez, Monica, Blanca Felipe-Abrio, and Patrizia Agostinis. "Mitophagy in Cancer: A Tale of Adaptation." Cells 8, no. 5 (May 22, 2019): 493. http://dx.doi.org/10.3390/cells8050493.
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In the past years, we have learnt that tumors co-evolve with their microenvironment, and that the active interaction between cancer cells and stromal cells plays a pivotal role in cancer initiation, progression and treatment response. Among the players involved, the pathways regulating mitochondrial functions have been shown to be crucial for both cancer and stromal cells. This is perhaps not surprising, considering that mitochondria in both cancerous and non-cancerous cells are decisive for vital metabolic and bioenergetic functions and to elicit cell death. The central part played by mitochondria also implies the existence of stringent mitochondrial quality control mechanisms, where a specialized autophagy pathway (mitophagy) ensures the selective removal of damaged or dysfunctional mitochondria. Although the molecular underpinnings of mitophagy regulation in mammalian cells remain incomplete, it is becoming clear that mitophagy pathways are intricately linked to the metabolic rewiring of cancer cells to support the high bioenergetic demand of the tumor. In this review, after a brief introduction of the main mitophagy regulators operating in mammalian cells, we discuss emerging cell autonomous roles of mitochondria quality control in cancer onset and progression. We also discuss the relevance of mitophagy in the cellular crosstalk with the tumor microenvironment and in anti-cancer therapy responses.
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Ferko, Miroslav, Natália Andelová, Barbara Szeiffová Bačová, and Magdaléna Jašová. "Myocardial Adaptation in Pseudohypoxia: Signaling and Regulation of mPTP via Mitochondrial Connexin 43 and Cardiolipin." Cells 8, no. 11 (November 17, 2019): 1449. http://dx.doi.org/10.3390/cells8111449.
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Therapies intended to mitigate cardiovascular complications cannot be applied in practice without detailed knowledge of molecular mechanisms. Mitochondria, as the end-effector of cardioprotection, represent one of the possible therapeutic approaches. The present review provides an overview of factors affecting the regulation processes of mitochondria at the level of mitochondrial permeability transition pores (mPTP) resulting in comprehensive myocardial protection. The regulation of mPTP seems to be an important part of the mechanisms for maintaining the energy equilibrium of the heart under pathological conditions. Mitochondrial connexin 43 is involved in the regulation process by inhibition of mPTP opening. These individual cardioprotective mechanisms can be interconnected in the process of mitochondrial oxidative phosphorylation resulting in the maintenance of adenosine triphosphate (ATP) production. In this context, the degree of mitochondrial membrane fluidity appears to be a key factor in the preservation of ATP synthase rotation required for ATP formation. Moreover, changes in the composition of the cardiolipin’s structure in the mitochondrial membrane can significantly affect the energy system under unfavorable conditions. This review aims to elucidate functional and structural changes of cardiac mitochondria subjected to preconditioning, with an emphasis on signaling pathways leading to mitochondrial energy maintenance during partial oxygen deprivation.
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Choudhury, Feroza K. "Mitochondrial Redox Metabolism: The Epicenter of Metabolism during Cancer Progression." Antioxidants 10, no. 11 (November 19, 2021): 1838. http://dx.doi.org/10.3390/antiox10111838.
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Mitochondrial redox metabolism is the central component in the cellular metabolic landscape, where anabolic and catabolic pathways are reprogrammed to maintain optimum redox homeostasis. During different stages of cancer, the mitochondrial redox status plays an active role in navigating cancer cells’ progression and regulating metabolic adaptation according to the constraints of each stage. Mitochondrial reactive oxygen species (ROS) accumulation induces malignant transformation. Once vigorous cell proliferation renders the core of the solid tumor hypoxic, the mitochondrial electron transport chain mediates ROS signaling for bringing about cellular adaptation to hypoxia. Highly aggressive cells are selected in this process, which are capable of progressing through the enhanced oxidative stress encountered during different stages of metastasis for distant colonization. Mitochondrial oxidative metabolism is suppressed to lower ROS generation, and the overall cellular metabolism is reprogrammed to maintain the optimum NADPH level in the mitochondria required for redox homeostasis. After reaching the distant organ, the intrinsic metabolic limitations of that organ dictate the success of colonization and flexibility of the mitochondrial metabolism of cancer cells plays a pivotal role in their adaptation to the new environment.
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Moyes, C. D., B. J. Battersby, and S. C. Leary. "Regulation of muscle mitochondrial design." Journal of Experimental Biology 201, no. 3 (February 1, 1998): 299–307. http://dx.doi.org/10.1242/jeb.201.3.299.
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Mitochondria are responsible for the generation of ATP to fuel muscle contraction. Hypermetabolic stresses imposed upon muscles can lead to mitochondrial proliferation, but the resulting mitochondria greatly resemble their progenitors. During the mitochondrial biogenesis that accompanies phenotypic adaptation, the stoichiometric relationships between functional elements are preserved through shared sensitivities of respiratory genes to specific transcription factors. Although the properties of muscle mitochondria are generally thought to be highly conserved across species, there are many examples of mitochondrial differences between muscle types, species and developmental states and even within single cells. In this review, we discuss (1) the nature and regulation of gene families that allow coordinated expression of genes for mitochondrial products and (2) the regulatory mechanisms by which mitochondrial differences can arise over physiological and evolutionary time.
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Keller, Amy C., Leslie A. Knaub, P. Mason McClatchey, Chelsea A. Connon, Ron Bouchard, Matthew W. Miller, Kate E. Geary, Lori A. Walker, Dwight J. Klemm, and Jane E. B. Reusch. "Differential Mitochondrial Adaptation in Primary Vascular Smooth Muscle Cells from a Diabetic Rat Model." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–15. http://dx.doi.org/10.1155/2016/8524267.
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Diabetes affects more than 330 million people worldwide and causes elevated cardiovascular disease risk. Mitochondria are critical for vascular function, generate cellular reactive oxygen species (ROS), and are perturbed by diabetes, representing a novel target for therapeutics. We hypothesized that adaptive mitochondrial plasticity in response to nutrient stress would be impaired in diabetes cellular physiology via a nitric oxide synthase- (NOS-) mediated decrease in mitochondrial function. Primary smooth muscle cells (SMCs) from aorta of the nonobese, insulin resistant rat diabetes model Goto-Kakizaki (GK) and the Wistar control rat were exposed to high glucose (25 mM). At baseline, significantly greater nitric oxide evolution, ROS production, and respiratory control ratio (RCR) were observed in GK SMCs. Upon exposure to high glucose, expression of phosphorylated eNOS, uncoupled respiration, and expression of mitochondrial complexes I, II, III, and V were significantly decreased in GK SMCs (p<0.05). Mitochondrial superoxide increased with high glucose in Wistar SMCs (p<0.05) with no change in the GK beyond elevated baseline concentrations. Baseline comparisons show persistent metabolic perturbations in a diabetes phenotype. Overall, nutrient stress in GK SMCs caused a persistent decline in eNOS and mitochondrial function and disrupted mitochondrial plasticity, illustrating eNOS and mitochondria as potential therapeutic targets.
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Vargas-Mendoza, Nancy, Marcelo Angeles-Valencia, Ángel Morales-González, Eduardo Osiris Madrigal-Santillán, Mauricio Morales-Martínez, Eduardo Madrigal-Bujaidar, Isela Álvarez-González, et al. "Oxidative Stress, Mitochondrial Function and Adaptation to Exercise: New Perspectives in Nutrition." Life 11, no. 11 (November 22, 2021): 1269. http://dx.doi.org/10.3390/life11111269.
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Cells have the ability to adapt to stressful environments as a part of their evolution. Physical exercise induces an increase of a demand for energy that must be met by mitochondria as the main (ATP) provider. However, this process leads to the increase of free radicals and the so-called reactive oxygen species (ROS), which are necessary for the maintenance of cell signaling and homeostasis. In addition, mitochondrial biogenesis is influenced by exercise in continuous crosstalk between the mitochondria and the nuclear genome. Excessive workloads may induce severe mitochondrial stress, resulting in oxidative damage. In this regard, the objective of this work was to provide a general overview of the molecular mechanisms involved in mitochondrial adaptation during exercise and to understand if some nutrients such as antioxidants may be implicated in blunt adaptation and/or an impact on the performance of exercise by different means.
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Nassef, Mohamed Zakaria, Jasmin E. Hanke, and Karsten Hiller. "Mitochondrial metabolism in macrophages." American Journal of Physiology-Cell Physiology 321, no. 6 (December 1, 2021): C1070—C1081. http://dx.doi.org/10.1152/ajpcell.00126.2021.
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Mitochondria are considered to be the powerhouse of the cell. Normal functioning of the mitochondria is not only essential for cellular energy production but also for several immunomodulatory processes. Macrophages operate in metabolic niches and rely on rapid adaptation to specific metabolic conditions such as hypoxia, nutrient limitations, or reactive oxygen species to neutralize pathogens. In this regard, the fast reprogramming of mitochondrial metabolism is indispensable to provide the cells with the necessary energy and intermediates to efficiently mount the inflammatory response. Moreover, mitochondria act as a physical scaffold for several proteins involved in immune signaling cascades and their dysfunction is immediately associated with a dampened immune response. In this review, we put special focus on mitochondrial function in macrophages and highlight how mitochondrial metabolism is involved in macrophage activation.
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Einer, Claudia, Simon Hohenester, Ralf Wimmer, Lena Wottke, Renate Artmann, Sabine Schulz, Christian Gosmann, et al. "Mitochondrial adaptation in steatotic mice." Mitochondrion 40 (May 2018): 1–12. http://dx.doi.org/10.1016/j.mito.2017.08.015.
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Landar, Aimee, Sruti Shiva, Anna-Liisa Levonen, Joo-Yeun Oh, Corinne Zaragoza, Michelle S. Johnson, and Victor M. Darley-Usmar. "Induction of the permeability transition and cytochrome c release by 15-deoxy-Δ12,14-prostaglandin J2 in mitochondria." Biochemical Journal 394, no. 1 (January 27, 2006): 185–95. http://dx.doi.org/10.1042/bj20051259.
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The electrophilic lipid 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) is known to allow adaptation to oxidative stress in cells at low concentrations and apoptosis at high levels. The mechanisms leading to adaptation involve the covalent modification of regul-atory proteins, such as Keap1, and augmentation of antioxidant defences in the cell. The targets leading to apoptosis are less well defined, but mitochondria have been indirectly implicated in the mechanisms of cell death mediated by electrophilic lipids. To determine the potential of electrophilic cyclopentenones to induce pro-apoptotic effects in the mitochondrion, we used isolated liver mitochondria and demonstrated that 15d-PGJ2 promotes Ca2+-induced mitochondrial swelling and cytochrome c release. The mechanisms involved are consistent with direct modification of protein thiols in the mitochondrion, rather than secondary formation of reactive oxygen species or lipid peroxidation. Using proteomic analysis in combination with biotinylated 15d-PGJ2, we were able to identify 17 potential targets of the electrophile-responsive proteome in isolated liver mitochondria. Taken together, these results suggest that electrophilic lipid oxidation products can target a sub-proteome in mitochondria, and this in turn results in the transduction of the electrophilic stimulus to the cell through cytochrome c release.
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Adhikari, Deepak, In-won Lee, Wai Shan Yuen, and John Carroll. "Oocyte mitochondria—key regulators of oocyte function and potential therapeutic targets for improving fertility." Biology of Reproduction 106, no. 2 (January 31, 2022): 366–77. http://dx.doi.org/10.1093/biolre/ioac024.
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Abstract The development of oocytes and early embryos is dependent on mitochondrial ATP production. This reliance on mitochondrial activity, together with the exclusively maternal inheritance of mitochondria in development, places mitochondria as central regulators of both fertility and transgenerational inheritance mechanisms. Mitochondrial mass and mtDNA content massively increase during oocyte growth. They are highly dynamic organelles and oocyte maturation is accompanied by mitochondrial trafficking around subcellular compartments. Due to their key roles in generation of ATP and reactive oxygen species (ROS), oocyte mitochondrial defects have largely been linked with energy deficiency and oxidative stress. Pharmacological treatments and mitochondrial supplementation have been proposed to improve oocyte quality and fertility by enhancing ATP generation and reducing ROS levels. More recently, the role of mitochondria-derived metabolites in controlling epigenetic modifiers has provided a mechanistic basis for mitochondria–nuclear crosstalk, allowing adaptation of gene expression to specific metabolic states. Here, we discuss the multi-faceted mechanisms by which mitochondrial function influence oocyte quality, as well as longer-term developmental events within and across generations.
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Kang, Ning, and Hongying Hu. "Adaptive evidence of mitochondrial genes in Pteromalidae and Eulophidae (Hymenoptera: Chalcidoidea)." PLOS ONE 18, no. 11 (November 21, 2023): e0294687. http://dx.doi.org/10.1371/journal.pone.0294687.
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Pteromalidae and Eulophidae are predominant and abundant taxa within Chalcidoidea (Hymenoptera: Apocrita). These taxa are found in diverse ecosystems, ranging from basin deserts (200 m) to alpine grasslands (4500 m). Mitochondria, cellular powerhouses responsible for energy production via oxidative phosphorylation, are sensitive to various environmental factors such as extreme cold, hypoxia, and intense ultraviolet radiation characteristic of alpine regions. Whether the molecular evolution of mitochondrial genes in these parasitoids corresponds to changes in the energy requirements and alpine environmental adaptations remains unknown. In this study, we performed a comparative analysis of mitochondrial protein-coding genes from 11 alpine species of Pteromalidae and Eulophidae, along with 18 lowland relatives, including 16 newly sequenced species. We further examined the codon usage preferences (RSCU, ENC-GC3s, neutrality, and PR2 bias plot) in these mitochondrial protein-coding sequences and conducted positive selection analysis based on their Bayesian phylogenetic relationships, and identified positive selection sites in the ATP6, ATP8, COX1, COX3, and CYTB genes, emphasizing the crucial role of mitochondrial gene adaptive evolution in the adaptation of Pteromalidae and Eulophidae to alpine environments. The phylogenetically independent contrast (PIC) analysis results verified the ω ratio of 13 PCGs from Pteromalidae and Eulophidae increased with elevation, and results from generalized linear model confirm that ATP6, ATP8, COX3, and ND1 are closely correlated with temperature-related environmental factors. This research not only enriched the molecular data of endemic alpine species but also underscores the significance of mitochondrial genes in facilitating the adaptation of these minor parasitoids to plateau habitats.
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Ojuka, Edward O. "Role of calcium and AMP kinase in the regulation of mitochondrial biogenesis and GLUT4 levels in muscle." Proceedings of the Nutrition Society 63, no. 2 (May 2004): 275–78. http://dx.doi.org/10.1079/pns2004339.
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Contractile activity induces mitochondrial biogenesis and increases glucose transport capacity in muscle. There has been much research on the mechanisms responsible for these adaptations. The present paper reviews the evidence, which indicates that the decrease in the levels of high-energy phosphates, leading to activation of AMP kinase (AMPK), and the increase in cytosolic Ca2+, which activates Ca2+/calmodulin-dependent protein kinase (CAMK), are signals that initiate these adaptative responses. Although the events downstream of AMPK and CAMK have not been well characterized, these events lead to activation of various transcription factors, including: nuclear respiratory factors (NRF) 1 and 2, which cause increased expression of proteins of the respiratory chain; PPAR-α, which up regulates the levels of enzymes of β oxidation; mitochondrial transcription factor A, which activates expression of the mitochondrial genome; myocyte-enhancing factor 2A, the transcription factor that regulates GLUT4 expression. The well-orchestrated expression of the multitude of proteins involved in these adaptations is mediated by the rapid activation of PPARγ co-activator (PGC) 1, a protein that binds to various transcription factors to maximize transcriptional activity. Activating AMPK using 5-aminoimidizole-4-carboxamide-1-β-D-riboside (AICAR) and increasing cytoplasmic Ca2+using caffeine, W7 or ionomycin in L6 myotubes increases the concentration of mitochondrial enzymes and GLUT4 and enhances the binding of NRF-1 and NRF-2 to DNA. AICAR and Ca-releasing agents also increase the levels of PGC-1, mitochondrial transcription factor A and myocyte-enhancing factors 2A and 2D. These results are similar to the responses seen in muscle during the adaptation to endurance exercise and show that L6 myotubes are a suitable model for studying the mechanisms by which exercise causes the adaptive responses in muscle mitochondria and glucose transport.
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Ždralević, Maša, Nicoletta Guaragnella, Lucia Antonacci, Ersilia Marra, and Sergio Giannattasio. "Yeast as a Tool to Study Signaling Pathways in Mitochondrial Stress Response and Cytoprotection." Scientific World Journal 2012 (2012): 1–10. http://dx.doi.org/10.1100/2012/912147.
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Cell homeostasis results from the balance between cell capability to adapt or succumb to environmental stress. Mitochondria, in addition to supplying cellular energy, are involved in a range of processes deciding about cellular life or death. The crucial role of mitochondria in cell death is well recognized. Mitochondrial dysfunction has been associated with the death process and the onset of numerous diseases. Yet, mitochondrial involvement in cellular adaptation to stress is still largely unexplored. Strong interest exists in pharmacological manipulation of mitochondrial metabolism and signaling. The yeastSaccharomyces cerevisiaehas proven a valuable model organism in which several intracellular processes have been characterized in great detail, including the retrograde response to mitochondrial dysfunction and, more recently, programmed cell death. In this paper we review experimental evidences of mitochondrial involvement in cytoprotection and propose yeast as a model system to investigate the role of mitochondria in the cross-talk between prosurvival and prodeath pathways.
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Costa, L. E., A. Boveris, O. R. Koch, and A. C. Taquini. "Liver and heart mitochondria in rats submitted to chronic hypobaric hypoxia." American Journal of Physiology-Cell Physiology 255, no. 1 (July 1, 1988): C123—C129. http://dx.doi.org/10.1152/ajpcell.1988.255.1.c123.
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Mitochondrial mass was determined in the heart and liver of rats submitted to 4,400 m (simulated altitude) for 9 mo and their controls at sea level. This was done 1) by evaluation of isolated mitochondrial protein per gram of tissue, 2) by evaluation of the ratio between cytochrome oxidase activity in tissue homogenate and in isolated mitochondria, and 3) by evaluation of mitochondrial numerical and volume density in fixed tissues analyzed by electron microscopy. An increase in mitochondrial mass and a more homogeneous distribution of mitochondria were found in liver. In cardiac tissue an increase in numerical density of mitochondria accompanied by a slight decrease in their mean volume was observed. Maximal physiological rate of mitochondrial respiration (state 3, active respiration), resting respiration, ADP/O, and acceptor control ratio were determined in the isolated mitochondria. No differences were found in the intrinsic properties of mitochondria. The results suggest that chronic mild hypoxia promotes tissue adaptation by increasing the mitochondrial mass or number in liver and heart, respectively, and improves intracellular O2 diffusion by adopting a more homogeneous intracellular distribution of mitochondria in the liver.
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Dunn, J. F. "Low-temperature adaptation of oxidative energy production in cold-water fishes." Canadian Journal of Zoology 66, no. 5 (May 1, 1988): 1098–104. http://dx.doi.org/10.1139/z88-161.
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This paper addresses the possibility that oxidative energy production in fish muscle is limited by low temperatures. Data are used from species that seasonally acclimatize to low temperatures, and from animals that have adapted to low temperatures over an evolutionary period. It is likely that the inhibitory effect of declining temperatures on the potential rate of oxidative energy production is compensated for largely by increasing the volume of mitochondria in the cell (volume density). For fishes that acclimatize, this increase in mitochondrial volume density may offset diffusion limitations. This is less likely for species that have adapted to low temperatures, because these animals have also developed large-diameter muscle cells. It is suggested that the stimuli for increasing cellular mitochondrial volume density, be they diffusion limitations or catalytic limitations, have not totally been overcome by increased mitochondrial volume density. In addition, a further restriction is concurrently placed upon maximum rates of oxygen uptake by the cell because the increase in mitochondrial volume density occurs at the expense of myofibrillar volume. This has the effect of reducing the maximum rate at which ATP can be used by working muscle.
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Joseph, Anna-Maria, Henriette Pilegaard, Anastassia Litvintsev, Lotte Leick, and David A. Hood. "Control of gene expression and mitochondrial biogenesis in the muscular adaptation to endurance exercise." Essays in Biochemistry 42 (November 27, 2006): 13–29. http://dx.doi.org/10.1042/bse0420013.
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Every time a bout of exercise is performed, a change in gene expression occurs within the contracting muscle. Over the course of many repeated bouts of exercise (i.e. training), the cumulative effects of these alterations lead to a change in muscle phenotype. One of the most prominent of these adaptations is an increase in mitochondrial content, which confers a greater resistance to muscle fatigue. This essay reviews current knowledge on the regulation of exercise-induced mitochondrial biogenesis at the molecular level. The major steps involved include, (i) transcriptional regulation of nuclear-encoded genes encoding mitochondrial proteins by the coactivator peroxisome-proliferator-activated receptor g coactivator-1, (ii) control of mitochondrial DNA gene expression by the transcription factor Tfam, (iii) mitochondrial fission and fusion mechanisms, and (iv) import of nuclear-derived gene products into the mitochondrion via the protein import machinery. It is now known that exercise can modify the rates of several of these steps, leading to mitochondrial biogenesis. An understanding of how exercise can produce this effect could help us decide whether exercise is beneficial for patients suffering from mitochondrial disorders, as well as a variety of metabolic diseases.
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Anand, Sanjeev K., and Suresh K. Tikoo. "Viruses as Modulators of Mitochondrial Functions." Advances in Virology 2013 (2013): 1–17. http://dx.doi.org/10.1155/2013/738794.
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Mitochondria are multifunctional organelles with diverse roles including energy production and distribution, apoptosis, eliciting host immune response, and causing diseases and aging. Mitochondria-mediated immune responses might be an evolutionary adaptation by which mitochondria might have prevented the entry of invading microorganisms thus establishing them as an integral part of the cell. This makes them a target for all the invading pathogens including viruses. Viruses either induce or inhibit various mitochondrial processes in a highly specific manner so that they can replicate and produce progeny. Some viruses encode the Bcl2 homologues to counter the proapoptotic functions of the cellular and mitochondrial proteins. Others modulate the permeability transition pore and either prevent or induce the release of the apoptotic proteins from the mitochondria. Viruses like Herpes simplex virus 1 deplete the host mitochondrial DNA and some, like human immunodeficiency virus, hijack the host mitochondrial proteins to function fully inside the host cell. All these processes involve the participation of cellular proteins, mitochondrial proteins, and virus specific proteins. This review will summarize the strategies employed by viruses to utilize cellular mitochondria for successful multiplication and production of progeny virus.
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Huang, Tai-Yu, Melissa A. Linden, Scott E. Fuller, Felicia R. Goldsmith, Jacob Simon, Heidi M. Batdorf, Matthew C. Scott, Nabil M. Essajee, John M. Brown, and Robert C. Noland. "Combined effects of a ketogenic diet and exercise training alter mitochondrial and peroxisomal substrate oxidative capacity in skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 320, no. 6 (June 1, 2021): E1053—E1067. http://dx.doi.org/10.1152/ajpendo.00410.2020.
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A ketogenic diet with normal protein content (NPKD) increases body weight and fat mass, increases intramuscular triglyceride storage, and upregulates pathways related to protein metabolism. In combination with exercise training, a NPKD induces additive and/or synergistic activation of AMPK, PGC-1α, mitochondrial fission/fusion genes, mitochondrial fatty acid oxidation, and peroxisomal adaptations in skeletal muscle. Collectively, results from this study provide mechanistic insight into adaptations in skeletal muscle relevant to keto-adaptation.
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Berner, Mariah J., Lily Baek, Junegoo Lee, Philip L. Lorenzi, Mei Leng, Alexander B. Saltzman, Anna Malovannaya, et al. "Abstract P6-11-10: Investigating the role of mitochondrial protein translation in the metabolic adaptation of chemoresistant triple negative breast cancer." Cancer Research 83, no. 5_Supplement (March 1, 2023): P6–11–10—P6–11–10. http://dx.doi.org/10.1158/1538-7445.sabcs22-p6-11-10.
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Abstract BACKGROUND: Nearly 50% of patients with triple negative breast cancer (TNBC) treated with neoadjuvant chemotherapy (NACT) retain residual tumors resulting in high rates of metastatic relapse and poor overall survival. Residual tumors surviving NACT (Adriamycin plus cyclophosphamide; AC) were found to undergo a metabolic transition to heightened mitochondrial oxidative phosphorylation (oxphos; PMID: 30996079). Pharmacologic inhibition of mitochondrial electron transport chain (ETC) complex I with IACS-010759 (PMID: 29892070) had enhanced efficacy in residual, rather than treatment-naïve, tumors of orthotopic patient-derived xenograft (PDX) models. Our analyses of mitochondrial structure and function in human TNBC cell lines revealed differing adaptations in residual cells surviving treatment with conventional NACT agents. While DNA-damaging chemotherapies (e.g.Adriamycin, carboplatin) induced mitochondrial fusion and oxphos, taxanes (e.g.paclitaxel, docetaxel) induced mitochondrial fragmentation and reduced oxphos (Baek et al., Biorxiv Doi 10.1101/2022.02.25.481996). The mechanistic basis of these mitochondrial adaptations is not yet understood. The mitochondrial ETC consists of 92 proteins, 13 of which are encoded in the mitochondrial genome (mtDNA) and translated by the mitoribosome, while the remaining are encoded by the nuclear genome (nDNA), translated by the cytoribosome, and inserted into the inner mitochondrial membrane by accessory proteins, namely Oxidase (Cytochrome C) Assembly 1-Like (OXA1L). Disruption of OXA1L in mammalian cells has been shown to affect the levels and activity of ETC complexes I, III, IV, and V, and thus diminish oxphos. We aim to determine whether mitochondrial translation and OXA1L activity represent therapeutic vulnerabilities to overcome pro-survival metabolic adaptations in chemoresistant TNBC thereby augmenting treatment response. METHODS: Weare evaluating the effects of conventional TNBC chemotherapies singly, and in standard combinations, on mitochondrial translation and ETC formation in human TNBC cells and PDX models(PIM001-P, WHIM14, BCM15116) using metabolomic and proteomic profiling. To perturb these processes genetically, we knocked down (KD) OXA1Lwith siRNA. We are complementing these studies pharmacologically using conventional antibiotics, such as tigecycline, as previous studies showed they inhibit mitochondrial translation in breast and other cancers (PMID: 25625193). These studies will reveal whether OXA1L and mitochondrial translation are required for metabolic adaption and chemotherapy resistance of residual TNBC cells. PDX preclinical trials based on our published residual tumor testing schema (PMID: 30996079), will reveal whether the sequential combination of NACT followed by tigecycline can effectively perturb residual tumor relapse. RESULTS: Proteomic profiling of longitudinally harvested PDX tumors demonstrates substantial disruption of mitochondria-and nuclear-encoded ETC components in residual vs. treatment-naïve tumors. Interestingly, these patterns are distinct between different chemotherapy treatments, with an increase of ETC components in carboplatin-treated residual tumors compared to a decrease in docetaxel-treated residual tumors. Western blot analyses of human cell lines show OXA1LKD perturbs levels of both nuclear-and mitochondria-encoded ETC components. Preliminary findings suggest OXA1LKD increases sensitivity to chemotherapies in human TNBC cell lines. Finally, tigecycline effectively inhibits TNBC cell growth. We next will evaluate whether residual cells not killed by conventional chemotherapies have enhanced tigecycline susceptibility. CONCLUSION: These data suggest targeting mitochondrial translation may be a promising approach to overcome pro-survival metabolic adaptations in residual TNBC cells not killed by conventional chemotherapies. Citation Format: Mariah J. Berner, Lily Baek, Junegoo Lee, Philip L. Lorenzi, Mei Leng, Alexander B. Saltzman, Anna Malovannaya, Lacey E. Dobrolecki, Christina Sallas, Michael T. Lewis, Gloria V. Echeverria. Investigating the role of mitochondrial protein translation in the metabolic adaptation of chemoresistant triple negative breast cancer [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr P6-11-10.
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Silva, Gonçalo, Fernando P. Lima, Paulo Martel, and Rita Castilho. "Thermal adaptation and clinal mitochondrial DNA variation of European anchovy." Proceedings of the Royal Society B: Biological Sciences 281, no. 1792 (October 7, 2014): 20141093. http://dx.doi.org/10.1098/rspb.2014.1093.
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Natural populations of widely distributed organisms often exhibit genetic clinal variation over their geographical ranges. The European anchovy, Engraulis encrasicolus , illustrates this by displaying a two-clade mitochondrial structure clinally arranged along the eastern Atlantic. One clade has low frequencies at higher latitudes, whereas the other has an anti-tropical distribution, with frequencies decreasing towards the tropics. The distribution pattern of these clades has been explained as a consequence of secondary contact after an ancient geographical isolation. However, it is not unlikely that selection acts on mitochondria whose genes are involved in relevant oxidative phosphorylation processes. In this study, we performed selection tests on a fragment of 1044 bp of the mitochondrial cytochrome b gene using 455 individuals from 18 locations. We also tested correlations of six environmental features: temperature, salinity, apparent oxygen utilization and nutrient concentrations of phosphate, nitrate and silicate, on a compilation of mitochondrial clade frequencies from 66 sampling sites comprising 2776 specimens from previously published studies. Positive selection in a single codon was detected predominantly (99%) in the anti-tropical clade and temperature was the most relevant environmental predictor, contributing with 59% of the variance in the geographical distribution of clade frequencies. These findings strongly suggest that temperature is shaping the contemporary distribution of mitochondrial DNA clade frequencies in the European anchovy.
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Blier, Pierre U., Hélène Lemieux, and Nicolas Pichaud. "Holding our breath in our modern world: will mitochondria keep the pace with climate changes?" Canadian Journal of Zoology 92, no. 7 (July 2014): 591–601. http://dx.doi.org/10.1139/cjz-2013-0183.
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Changes in environmental temperature can pose considerable challenges to animals and shifts in thermal habitat have been shown to be a major force driving species’ adaptation. These adaptations have been the focus of major research efforts to determine the physiological or metabolic constraints related to temperature and to reveal the phenotypic characters that can or should adjust. Considering the current consensus on climate change, the focus of research will likely shift to questioning whether ectothermic organisms will be able to survive future modifications of their thermal niches. Organisms can adjust to temperature changes through physiological plasticity (e.g., acclimation), genetic adaptation, or via dispersal to more suitable thermal habitats. Thus, it is important to understand what genetic and phenotypic attributes—at the individual, population, and species levels—could improve survival success. These issues are particularly important for ectotherms, which are in thermal equilibrium with the surrounding environment. To start addressing these queries, we should consider what physiological or metabolic functions are responsible for the impact of temperature on organisms. Some recent developments indicate that mitochondria are key metabolic structures determining the thermal range that an organism can tolerate. The catalytic capacity of mitochondria is highly sensitive to thermal variation and therefore should partly dictate the temperature dependence of biological functions. Mitochondria contain a complex network of different enzymatic reaction pathways that interact synergistically. The precise regulation of both adenosine triphosphate (ATP) and reactive oxygen species (ROS) production depends on the integration of different enzymes and pathways. Here, we examine the temperature dependence of different parts of mitochondrial pathways and evaluate the evolutionary challenges that need to be overcome to ensure mitochondrial adaptations to new thermal environments.
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Finocchietto, Paola V., Maria C. Franco, Silvia Holod, Analia S. Gonzalez, Daniela P. Converso, Valeria G. Antico Arciuch, Maria P. Serra, Juan J. Poderoso, and Maria C. Carreras. "Mitochondrial Nitric Oxide Synthase: A Masterpiece of Metabolic Adaptation, Cell Growth, Transformation, and Death." Experimental Biology and Medicine 234, no. 9 (September 2009): 1020–28. http://dx.doi.org/10.3181/0902-mr-81.
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Mitochondria are specialized organelles that control energy metabolism and also activate a multiplicity of pathways that modulate cell proliferation and mitochondrial biogenesis or, conversely, promote cell arrest and programmed cell death by a limited number of oxidative or nitrative reactions. Nitric oxide (NO) regulates oxygen uptake by reversible inhibition of cytochrome oxidase and the production of superoxide anion from the mitochondrial electron transfer chain. In this sense, NO produced by mtNOS will set the oxygen uptake level and contribute to oxidation-reduction reaction (redox)–dependent cell signaling. Modulation of translocation and activation of neuronal nitric oxide synthase (mtNOS activity) under different physiologic or pathologic conditions represents an adaptive response properly modulated to adjust mitochondria to different cell challenges.
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Hafen, Paul S., Coray N. Preece, Jacob R. Sorensen, Chad R. Hancock, and Robert D. Hyldahl. "Repeated exposure to heat stress induces mitochondrial adaptation in human skeletal muscle." Journal of Applied Physiology 125, no. 5 (November 1, 2018): 1447–55. http://dx.doi.org/10.1152/japplphysiol.00383.2018.
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The heat stress response is associated with several beneficial adaptations that promote cell health and survival. Specifically, in vitro and animal investigations suggest that repeated exposures to a mild heat stress (~40°C) elicit positive mitochondrial adaptations in skeletal muscle comparable to those observed with exercise. To assess whether such adaptations translate to human skeletal muscle, we produced local, deep tissue heating of the vastus lateralis via pulsed shortwave diathermy in 20 men and women ( n = 10 men; n = 10 women). Diathermy increased muscle temperature by 3.9°C within 30 min of application. Immediately following a single 2-h heating session, we observed increased phosphorylation of AMP-activated protein kinase and ERK1/2 but not of p38 MAPK or JNK. Following repeated heat exposures (2 h daily for 6 consecutive days), we observed a significant cellular heat stress response, as heat shock protein 70 and 90 increased 45% and 38%, respectively. In addition, peroxisome proliferator-activated receptor gamma, coactivator-1 alpha and mitochondrial electron transport protein complexes I and V expression were increased after heating. These increases were accompanied by augmentation of maximal coupled and uncoupled respiratory capacity, measured via high-resolution respirometry. Our data provide the first evidence that mitochondrial adaptation can be elicited in human skeletal muscle in response to repeated exposures to mild heat stress. NEW & NOTEWORTHY Heat stress has been shown to elicit mitochondrial adaptations in cell culture and animal research. We used pulsed shortwave diathermy to produce deep tissue heating and explore whether beneficial mitochondrial adaptations would translate to human skeletal muscle in vivo. We report, for the first time, positive mitochondrial adaptations in human skeletal muscle following recurrent heat stress. The results of this study have clinical implications for many conditions characterized by diminished skeletal muscle mitochondrial function.
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Fratianni, Alessandra, Donato Pastore, Maria Luigia Pallotta, Donato Chiatante, and Salvatore Passarella. "Increase of Membrane Permeability of Mitochondria Isolated from Water Stress Adapted Potato Cells." Bioscience Reports 21, no. 1 (February 1, 2001): 81–91. http://dx.doi.org/10.1023/a:1010490219357.
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In order to gain some insight into mitochondria permeability under water stress, intact coupled mitochondria were isolated from water stress adapted potato cells and investigations were made of certain transport processes including the succinate/malate and ADP/ATP exchanges, the plant mitochondrial ATP-sensitive potassium channel (PmitoKATP) and the plant uncoupling mitochondrial protein (PUMP). The VmaxL values measured for succinate/malate and ADP/ATP carriers, as photometrically investigated, as well as the same values for the PmitoATP and the PUMP were found to increase; this suggested that mitochondria adaptation to water stress can cause an increase in the membrane permeability.
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KLINGENSPOR, Martin, Marc IVEMEYER, Herbert WIESINGER, Kirsten HAAS, Gerhard HELDMAIER, and Rudolf J. WIESNER. "Biogenesis of thermogenic mitochondria in brown adipose tissue of Djungarian hamsters during cold adaptation." Biochemical Journal 316, no. 2 (June 1, 1996): 607–13. http://dx.doi.org/10.1042/bj3160607.
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After cold exposure, cytochrome c oxidase (COX) activity increased about 2.5-fold within 2 weeks in the brown adipose tissue (BAT) of Djungarian hamsters. The mRNAs for COX subunits I and III and the 12 S rRNA, encoded on mitochondrial DNA (mtDNA), as well as mRNAs for COX subunits IV, Va and mitochondrial transcription factor A, encoded in the nucleus, were unchanged when expressed per unit of total tissue RNA. However, since total tissue RNA doubled per BAT depot, while total DNA remained unchanged, the actual levels of these transcripts were increased within BAT cells. In contrast, the abundance of mRNA for uncoupling protein was increased 10-fold, indicating specific activation of this gene. In addition, the maximal rate of protein synthesis analysed in a faithful in organello system was increased 2.5-fold in mitochondria isolated from BAT after 7 days of cold exposure. We conclude from these data that the biogenesis of thermogenic mitochondria in BAT following cold adaptation is achieved by increasing the overall capacity for synthesis of mitochondrial proteins in both compartments, by increasing their mRNAs as well as the ribosomes needed for their translation. In addition, the translational rate for COX subunits as well as all other proteins encoded on mtDNA is increased. Thus the pool of subunits encoded on mtDNA required for assembly of respiratory chain complexes is provided. By comparison with other models of increased mitochondrial biogenesis, we propose that thyroid hormone (generated within BAT cells by 5´-deiodinase, and induced upon sympathetic stimulation), which is a well known regulator of the biogenesis of mitochondria in many tissues, is also the major effector of these adaptive changes in BAT.
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Rafael, J., W. Fesser, and D. G. Nicholls. "Cold adaptation in guinea pig at level of isolated brown adipocyte." American Journal of Physiology-Cell Physiology 250, no. 2 (February 1, 1986): C228—C235. http://dx.doi.org/10.1152/ajpcell.1986.250.2.c228.
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Isolated brown adipocytes were prepared from guinea pigs acclimated to 28 degrees C or exposed to 4-8 degrees C for periods of up to 3 wk. Cells from warm-adapted animals retained respiratory control when stimulated with norepinephrine. Cells from guinea pigs exposed to cold for 4-21 days showed a much greater respiratory response to norepinephrine due to enhanced uncoupling rather than enhanced substrate supply. After 7 days of cold acclimation, norepinephrine-stimulated respiration became uncontrolled and was limited only by the maximal respiratory capacity of the mitochondria. Three weeks of cold acclimation were accompanied by a doubling of total cell number, a doubling of the mitochondrial protein per adipocyte, and a sixfold increase in the norepinephrine-stimulated respiration per in situ mitochondrion with no change in respiratory chain capacity. The induction of norepinephrine-stimulated respiration correlated with the appearance of high-affinity purine nucleotide binding sites on the mitochondria, diagnostic of the uncoupling protein. If the results are extrapolated to the whole animal, they indicate that brown adipose tissue makes little contribution to thermogenesis in the warm-adapted guinea pig but may account for most or all the increment seen on cold adaptation.
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Lou, Han, Henghui Xu, and Yong Zhang. "FAM210A: Implications in mitochondrial dynamics and metabolic health." Frigid Zone Medicine 3, no. 4 (December 1, 2023): 196–98. http://dx.doi.org/10.2478/fzm-2023-0025.
Full textAbstract:
Abstract Brown adipose tissue (BAT), crucial for mammalian thermoregulation and energy metabolism, boasts a dense concentration of mitochondria. As a vital cellular organelle, mitochondria undergo substantial remodeling in cold environments, playing a pivotal role in maintaining body temperature and energy balance[1]. Mitochondrial dynamics, particularly mitochondrial cristae remodeling, are key processes governing BAT functionality. A recent study by Qiu et al. unveils groundbreaking insights, highlighting the significance of FAM210A (family with sequence similarity 210 member A) in orchestrating cold-induced mitochondrial remodeling in brown adipocytes. This research sheds light on the molecular mechanisms underpinning mitochondrial adaptability in cold environments[2]. Central to these discoveries is the protein FAM210A, recognized as a critical regulator of mitochondrial cristae remodeling in BAT. This revelation introduces new perspectives on metabolic regulation and thermogenic adaptation. This editorial aims to dissect these findings, extrapolating their broader implications for understanding metabolic health. Additionally, it explores potential therapeutic targets and discusses future directions in mitochondrial research.
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Novikov, Vasiliy Egorovich, and Olga Sergeevna Levchenkova. "Mitochondrial targets for pharmacological regulation of cell adaptation to hypoxia." Reviews on Clinical Pharmacology and Drug Therapy 12, no. 2 (June 15, 2014): 28–35. http://dx.doi.org/10.17816/rcf12228-35.
Full textAbstract:
The review is devoted to the role of a number of mitochondrial factors in the regulation of cell adaptation to hypoxia and ischemia. The mechanisms of cell adaptation involving factors such as the mitochondrial ATP-dependent potassium channel, mitochondrial megapora, mitochondrial nitric oxide synthase, reactive oxygen species are discussed in the paper. The possibility of pharmacological regulation of cell adaptation with help of target action on mitochondrial components is proposed. This approach is a promising direction for drug discovery for correction of diseases with hypoxia and ischemia in their pathogenesis.
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Delcourt, Manon, Virginie Delsinne, Jean-Marie Colet, Anne-Emilie Declèves, and Vanessa Tagliatti. "Investigation of Mitochondrial Adaptations to Modulation of Carbohydrate Supply during Adipogenesis of 3T3-L1 Cells by Targeted 1H-NMR Spectroscopy." Biomolecules 11, no. 5 (April 29, 2021): 662. http://dx.doi.org/10.3390/biom11050662.
Full textAbstract:
(1) Background: White adipose tissue (WAT) is a dynamic and plastic tissue showing high sensitivity to carbohydrate supply. In such a context, the WAT may accordingly modulate its mitochondrial metabolic activity. We previously demonstrated that a partial replacement of glucose by galactose in a culture medium of 3T3-L1 cells leads to a poorer adipogenic yield and improved global mitochondrial health. In the present study, we investigate key mitochondrial metabolic actors reflecting mitochondrial adaptation in response to different carbohydrate supplies. (2) Methods: The metabolome of 3T3-L1 cells was investigated during the differentiation process using different glucose/galactose ratios and by a targeted approach using 1H-NMR (Proton nuclear magnetic resonance) spectroscopy; (3) Results: Our findings indicate a reduction of adipogenic and metabolic overload markers under the low glucose/galactose condition. In addition, a remodeling of the mitochondrial function triggers the secretion of metabolites with signaling and systemic energetical homeostasis functions. Finally, this study also sheds light on a new way to consider the mitochondrial metabolic function by considering noncarbohydrates related pathways reflecting both healthier cellular and mitochondrial adaptation mechanisms; (4) Conclusions: Different carbohydrates supplies induce deep mitochondrial metabolic and function adaptations leading to overall adipocytes function and profile remodeling during the adipogenesis.
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Wu, Ne N., Yingmei Zhang, and Jun Ren. "Mitophagy, Mitochondrial Dynamics, and Homeostasis in Cardiovascular Aging." Oxidative Medicine and Cellular Longevity 2019 (November 4, 2019): 1–15. http://dx.doi.org/10.1155/2019/9825061.
Full textAbstract:
Biological aging is an inevitable and independent risk factor for a wide array of chronic diseases including cardiovascular and metabolic diseases. Ample evidence has established a pivotal role for interrupted mitochondrial homeostasis in the onset and development of aging-related cardiovascular anomalies. A number of culprit factors have been suggested in aging-associated mitochondrial anomalies including oxidative stress, lipid toxicity, telomere shortening, metabolic disturbance, and DNA damage, with recent findings revealing a likely role for compromised mitochondrial dynamics and mitochondrial quality control machinery such as autophagy. Mitochondria undergo consistent fusion and fission, which are crucial for mitochondrial homeostasis and energy adaptation. Autophagy, in particular, mitochondria-selective autophagy, namely, mitophagy, refers to a highly conservative cellular process to degrade and clear long-lived or damaged cellular organelles including mitochondria, the function of which gradually deteriorates with increased age. Mitochondrial homeostasis could be achieved through a cascade of independent but closely related processes including fusion, fission, mitophagy, and mitochondrial biogenesis. With improved health care and increased human longevity, the ever-rising aging society has imposed a high cardiovascular disease prevalence. It is thus imperative to understand the role of mitochondrial homeostasis in the regulation of lifespan and healthspan. Targeting mitochondrial homeostasis should offer promising novel therapeutic strategies against aging-related complications, particularly cardiovascular diseases.
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Song, Jinxing, Jingwen Zhou, Lei Zhang, and Rongpeng Li. "Mitochondria-Mediated Azole Drug Resistance and Fungal Pathogenicity: Opportunities for Therapeutic Development." Microorganisms 8, no. 10 (October 13, 2020): 1574. http://dx.doi.org/10.3390/microorganisms8101574.
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In recent years, the role of mitochondria in pathogenic fungi in terms of azole resistance and fungal pathogenicity has been a rapidly developing field. In this review, we describe the molecular mechanisms by which mitochondria are involved in regulating azole resistance and fungal pathogenicity. Mitochondrial function is involved in the regulation of drug efflux pumps at the transcriptional and posttranslational levels. On the one hand, defects in mitochondrial function can serve as the signal leading to activation of calcium signaling and the pleiotropic drug resistance pathway and, therefore, can globally upregulate the expression of drug efflux pump genes, leading to azole drug resistance. On the other hand, mitochondria also contribute to azole resistance through modulation of drug efflux pump localization and activity. Mitochondria further contribute to azole resistance through participating in iron homeostasis and lipid biosynthesis. Additionally, mitochondrial dynamics play an important role in azole resistance. Meanwhile, mitochondrial morphology is important for fungal virulence, playing roles in growth in stressful conditions in a host. Furthermore, there is a close link between mitochondrial respiration and fungal virulence, and mitochondrial respiration plays an important role in morphogenetic transition, hypoxia adaptation, and cell wall biosynthesis. Finally, we discuss the possibility for targeting mitochondrial factors for the development of antifungal therapies.
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Tripathi, Kuldeep, and Dorit Ben-Shachar. "Mitochondria in the Central Nervous System in Health and Disease: The Puzzle of the Therapeutic Potential of Mitochondrial Transplantation." Cells 13, no. 5 (February 27, 2024): 410. http://dx.doi.org/10.3390/cells13050410.
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Mitochondria, the energy suppliers of the cells, play a central role in a variety of cellular processes essential for survival or leading to cell death. Consequently, mitochondrial dysfunction is implicated in numerous general and CNS disorders. The clinical manifestations of mitochondrial dysfunction include metabolic disorders, dysfunction of the immune system, tumorigenesis, and neuronal and behavioral abnormalities. In this review, we focus on the mitochondrial role in the CNS, which has unique characteristics and is therefore highly dependent on the mitochondria. First, we review the role of mitochondria in neuronal development, synaptogenesis, plasticity, and behavior as well as their adaptation to the intricate connections between the different cell types in the brain. Then, we review the sparse knowledge of the mechanisms of exogenous mitochondrial uptake and describe attempts to determine their half-life and transplantation long-term effects on neuronal sprouting, cellular proteome, and behavior. We further discuss the potential of mitochondrial transplantation to serve as a tool to study the causal link between mitochondria and neuronal activity and behavior. Next, we describe mitochondrial transplantation’s therapeutic potential in various CNS disorders. Finally, we discuss the basic and reverse—translation challenges of this approach that currently hinder the clinical use of mitochondrial transplantation.