Relevant bibliographies by topics / Mitochondrial medicine

Academic literature on the topic 'Mitochondrial medicine'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Mitochondrial medicine"

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Weissig, Volkmar, and Marvin Edeas. "Recent developments in mitochondrial medicine (Part 1)." 4open 4 (2021): 2. http://dx.doi.org/10.1051/fopen/2021002.

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Research into elucidating structure and function of mitochondria has been quite steady between the time of discovery during the end of the 19th century until towards the late 1980’s. During the 1990s there was talk about a “comeback” of this organelle reflecting a widely revitalized interest into mitochondrial research which was based on two major discoveries made during that time. The first was the etiological association between human diseases and mitochondrial DNA mutations, while the second revealed the crucial function of mitochondria during apoptosis. The March 5th, 1999 issue of Science even featured a textbook image of a mitochondrion on its front cover and was entirely dedicated to this organelle. Whilst the term “comeback” might have been appropriate to describe the general excitement surrounding the new mitochondrial discoveries made during the 1990s, a term for describing the progress made in mitochondrial research during the last two decades is difficult to find. Between 2000 and 2020 the number of publications on mitochondria has skyrocketed. It is now widely accepted that there hardly exists any human disease for which either the etiology or pathogenesis does not seem to be associated with mitochondrial malfunction. In this review we will discuss and follow several lines of mitochondrial research from their early beginnings up to the present. We hope to be able to convince the reader of what we expressed about a decade ago, that the future of medicine will come through mitochondria.
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Weissig, Volkmar, and Marvin Edeas. "Recent developments in mitochondrial medicine (part 2)." 4open 5 (2022): 5. http://dx.doi.org/10.1051/fopen/2022002.

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Called “bioblasts” in 1890, named “mitochondria” in 1898, baptized in 1957 as the “powerhouse of the cell” and christened in 1999 as the “motor of cell death”, mitochondria have been anointed in 2017 as “powerhouses of immunity”. In 1962, for the first time a causal link between mitochondria and human diseases was described, the genetic basis for which was revealed in 1988. The term “mitochondrial medicine” was coined in 1994. Research into mitochondria has been conducted ever since light microscopic studies during the end of the 19th century revealed their existence. To this day, new discoveries around this organelle and above all new insights into their fundamental role for human health and disease continue to surprise. Nowadays hardly any disease is known for which either the etiology or pathogenesis is not associated with malfunctioning mitochondria. In this second part of our review about recent developments in mitochondrial medicine we continue tracking and highlighting selected lines of mitochondrial research from their beginnings up to the present time. Mainly written for readers not familiar with this cell organelle, we hope both parts of our review will substantiate what we articulated over a decade ago, namely that the future of medicine will come through better understanding of the mitochondrion.
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D’Amato, Marco, Francesca Morra, Ivano Di Di Meo, and Valeria Tiranti. "Mitochondrial Transplantation in Mitochondrial Medicine: Current Challenges and Future Perspectives." International Journal of Molecular Sciences 24, no. 3 (January 19, 2023): 1969. http://dx.doi.org/10.3390/ijms24031969.

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Mitochondrial diseases (MDs) are inherited genetic conditions characterized by pathogenic mutations in nuclear DNA (nDNA) or mitochondrial DNA (mtDNA). Current therapies are still far from being fully effective and from covering the broad spectrum of mutations in mtDNA. For example, unlike heteroplasmic conditions, MDs caused by homoplasmic mtDNA mutations do not yet benefit from advances in molecular approaches. An attractive method of providing dysfunctional cells and/or tissues with healthy mitochondria is mitochondrial transplantation. In this review, we discuss what is known about intercellular transfer of mitochondria and the methods used to transfer mitochondria both in vitro and in vivo, and we provide an outlook on future therapeutic applications. Overall, the transfer of healthy mitochondria containing wild-type mtDNA copies could induce a heteroplasmic shift even when homoplasmic mtDNA variants are present, with the aim of attenuating or preventing the progression of pathological clinical phenotypes. In summary, mitochondrial transplantation is a challenging but potentially ground-breaking option for the treatment of various mitochondrial pathologies, although several questions remain to be addressed before its application in mitochondrial medicine.
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Wang, Jie, Fei Lin, Li-li Guo, Xing-jiang Xiong, and Xun Fan. "Cardiovascular Disease, Mitochondria, and Traditional Chinese Medicine." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/143145.

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Recent studies demonstrated that mitochondria play an important role in the cardiovascular system and mutations of mitochondrial DNA affect coronary artery disease, resulting in hypertension, atherosclerosis, and cardiomyopathy. Traditional Chinese medicine (TCM) has been used for thousands of years to treat cardiovascular disease, but it is not yet clear how TCM affects mitochondrial function. By reviewing the interactions between the cardiovascular system, mitochondrial DNA, and TCM, we show that cardiovascular disease is negatively affected by mutations in mitochondrial DNA and that TCM can be used to treat cardiovascular disease by regulating the structure and function of mitochondria via increases in mitochondrial electron transport and oxidative phosphorylation, modulation of mitochondrial-mediated apoptosis, and decreases in mitochondrial ROS. However further research is still required to identify the mechanism by which TCM affects CVD and modifies mitochondrial DNA.
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Kiseljaković, Emina, Radivoj Jadrić, Sabaheta Hasić, Lorenka Ljuboja, Jovo Radovanović, Husein Kulenović, and Mira Winterhalter-Jadrić. "Mitochondrial medicine - a key to solve pathophysiology of 21 century diseases." Bosnian Journal of Basic Medical Sciences 2, no. 1-2 (February 20, 2008): 46–48. http://dx.doi.org/10.17305/bjbms.2002.3580.

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Over the past 13 years mitochondrial defects have been involved in wide variety of degenerative diseases - Parkinson disease, Alzheimer dementia, arteriosclerosis, ageing and cancer. Mitochondria are believed to control apoptosis or programmed cell death. Disturbance in mitochondrial metabolism has also been implicated in many common diseases such as congestive hart failure, diabetes and migraine. Scientific investigations have showed complexities in mitochondrial genetics, but at the same time, pathophysiology of mitochondrial diseases is still enigma. Mitochondria and their DNAs are opening the era of "mitochondrial medicine". What we today call "a mitochondrial medicine" is only a part of the whole panorama of diseases based on disordered mitochondrial function.
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Qin, Lingyu, and Shuhua Xi. "The role of Mitochondrial Fission Proteins in Mitochondrial Dynamics in Kidney Disease." International Journal of Molecular Sciences 23, no. 23 (November 25, 2022): 14725. http://dx.doi.org/10.3390/ijms232314725.

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Mitochondria have many forms and can change their shape through fusion and fission of the outer and inner membranes, called “mitochondrial dynamics”. Mitochondrial outer membrane proteins, such as mitochondrial fission protein 1 (FIS1), mitochondrial fission factor (MFF), mitochondrial 98 dynamics proteins of 49 kDa (MiD49), and mitochondrial dynamics proteins of 51 kDa (MiD51), can aggregate at the outer mitochondrial membrane and thus attract Dynamin-related protein 1 (DRP1) from the cytoplasm to the outer mitochondrial membrane, where DRP1 can perform a scissor-like function to cut a complete mitochondrion into two separate mitochondria. Other organelles can promote mitochondrial fission alongside mitochondria. FIS1 plays an important role in mitochondrial–lysosomal contacts, differentiating itself from other mitochondrial-fission-associated proteins. The contact between the two can also induce asymmetric mitochondrial fission. The kidney is a mitochondria-rich organ, requiring large amounts of mitochondria to produce energy for blood circulation and waste elimination. Pathological increases in mitochondrial fission can lead to kidney damage that can be ameliorated by suppressing their excessive fission. This article reviews the current knowledge on the key role of mitochondrial-fission-associated proteins in the pathogenesis of kidney injury and the role of their various post-translational modifications in activation or degradation of fission-associated proteins and targeted drug therapy.
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Michelakis, Evangelos D. "Mitochondrial Medicine." Circulation 117, no. 19 (May 13, 2008): 2431–34. http://dx.doi.org/10.1161/circulationaha.108.775163.

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Chinnery, P. F., and D. M. Turnbull. "Mitochondrial medicine." QJM 90, no. 11 (November 1, 1997): 657–67. http://dx.doi.org/10.1093/qjmed/90.11.657.

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Dorey, Emma. "Mitochondrial medicine." Nature Biotechnology 32, no. 4 (April 2014): 300. http://dx.doi.org/10.1038/nbt0414-300a.

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Luft, Rolf, and B. R. LANDAU. "Mitochondrial medicine." Journal of Internal Medicine 238, no. 5 (November 1995): 405–21. http://dx.doi.org/10.1111/j.1365-2796.1995.tb01218.x.

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Dissertations / Theses on the topic "Mitochondrial medicine"

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Das, Gupta Fenella. "Mitochondrial involvement in models of schizophrenia." Thesis, King's College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265112.

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Forrester, Steven James. "MITOCHONDRIA FACILITATE VASCULAR INFLAMMATION: THE ROLE OF CANONICAL INFLAMMATORY SIGNALING IN THE REGULATION OF MITOCHONDRIAL MORPHOLOGY." Diss., Temple University Libraries, 2017. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/429386.

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Kinesiology
Ph.D.
Vascular inflammation is an underlying cause to numerous diseases and is characterized by classical NF-κB activation and downstream physiological responses including inflammatory gene induction and immune cell recruitment. Although inflammatory based diseases are associated with mitochondrial dysfunction and morphological alterations, the direct mechanisms tying the mitochondria to canonical NF-κB signaling remain elusive. Using pharmacological and genetic approaches, we show inflammatory-mediated mitochondrial fission, through DRP1 and MFF, is required for NF-κB activation, VCAM-1 induction and vascular inflammation in vitro and in vivo. In addition, inflammatory signaling in the endothelium mediates mitochondrial fission through an IKKβ/IκBα-dependent pathway. IκBα is found to localize on the mitochondrial outer membrane where it inhibits DRP1 recruitment to the mitochondria. Inhibition of this cascade promotes elongated mitochondria that are unable to go through fission. Cumulatively, these results highlight the requirement of mitochondrial fission in the inflammatory response. Our results point to a shift in how classical NF-κB induction and downstream inflammatory signaling is viewed, as well as highlights a new inflammatory-dependent mechanism in mitochondrial dynamics. This work also suggests a link between inflammatory-based diseases of different etiologies and a conserved mitochondrial fission pathway.
Temple University--Theses
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Hershman, Steven Gregory. "Personal Genomics and Mitochondrial Disease." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:10863.

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Mitochondrial diseases involving dysfunction of the respiratory chain are the most common inborn errors of metabolism. Mitochondria are found in all cell types besides red blood cells; consequently, patients can present with any symptom in any organ at any age. These diseases are genetically heterogeneous, and exhibit maternal, autosomal dominant, autosomal recessive and X-linked modes of inheritance. Historically, clinical genetic evaluation of mitochondrial disease has been limited to sequencing of the mitochondrial DNA (mtDNA) or several candidate genes. As human genome sequencing transformed from a research grade effort costing $250,000 to a clinical test orderable by doctors for under $10,000, it has become practical for researchers to sequence individual patients. This thesis describes our experiences in applying "MitoExome" sequencing of the mtDNA and exons of >1000 nuclear genes encoding mitochondrial proteins in ~200 patients with suspected mitochondrial disease. In 42 infants, we found that 55% harbored pathogenic mtDNA variants or compound heterozygous mutations in candidate genes. The pathogenicity of two nuclear genes not previously linked to disease, NDUFB3 and AGK, was supported by complementation studies and evidence from multiple patients, respectively. In an additional two unrelated children presenting with Leigh syndrome and combined OXPHOS deficiency, we identified compound heterozygous mutations in MTFMT. Patient fibroblasts exhibit severe defects in mitochondrial translation that can be rescued by exogenous expression of MTFMT. Furthermore, patient fibroblasts have dramatically reduced fMet-\(tRNA^{Met}\) levels and an abnormal formylation profile of mitochondrially translated \(COX_1\). These results demonstrate that MTFMT is critical for human mitochondrial translation. Lastly, to facilitate evaluation of copy number variants (CNVs), we developed a web-interface that integrates CNV calling with genetic and phenotypic information. Additional diagnoses are suggested and in a male with ataxia, neuropathy, azoospermia, and hearing loss we found a deletion compounded with a missense variant in D-bifunctional protein, \(HSD_{17}B_4\), a peroxisomal enzyme that catalyzes beta-oxidation of very long chain fatty acids. Retrospective review of metabolic testing from this patient revealed alterations of long- and very-long chain fatty acid metabolism consistent with a peroxisomal disorder. This work expands the molecular basis of mitochondrial disease and has implications for clinical genomics.
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Ryan, Margaret Mary. "An investigation into mitochondrial sequence variation and schizophrenia." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270543.

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Chan, Wing Yin Anna. "Cardiac mitochondrial respiration in two rodent models of obesity." Master's thesis, University of Cape Town, 2006. http://hdl.handle.net/11427/3371.

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Includes bibliographical references (leaves 95-107)
Obesity is a major contributor to the global burden of disease and is closely associated with the development of type II diabetes. Recent studies have demonstrated that increased circulating free fatty acid (FFA) levels may have detrimental effects on the diabetic heart. In this study, we hypothesized that with obesity and obesity-induced insulin resistance/type II diabetes, increased FFA supply decreases cardiac mitochondrial bioenergetic capacity. Furthermore, we also hypothesized that females possess innate cardioprotective programs that will result in enhanced bioenergetic capacity compared to males. We examined our hypothesis employing two rodent models i.e. a) a rat model of diet-induced obesity and b) a transgenic (leptin receptor deficient) mouse model of obesity-induced type II diabetes. For the diabetic mouse model, we determined cardiac mitochondrial respiratory function in an age-dependent (10-12, 18-20 and 55-56 weeks) and gender-dependent (male versus female) manner. We found impaired mitochondrial respiratory capacity in obese rats in baseline and when isolated mitochondria were stressed by anoxia-reoxygenation. We speculate that this may be dure to reduced expression of mitochondrial respiratory chain complexes in the insulin resistant rat heart. For the mouse model and type II diabetes we found increased respiratory capacity at 10-12 weeks, thought to respresent the stage of metabolic syndrome, with no evidence of oxygen wastage or reduction of respiratory capacity. However, 18-20 week-old obese mice were unable to increase respiratory capacity. We also found increased mitochondrial ultrastructural damage and intracellular lipid accumulation in 18-20 week-old diabetic mouse hearts. We propose that this occurs as a result of a mismatch between increased FA uptake and decreased FA oxidative capacity.
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Laskowski, Karl Robert. "The regulation of mitochondrial uncoupling proteins in the heart." [New Haven, Conn. : s.n.], 2008. http://ymtdl.med.yale.edu/theses/available/etd-12082008-103644.

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Ruchala, Monika. "Mitochondrial Gene Expression in Human Mononuclear Cells." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/3530.

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MITOCHONDRIAL GENE EXPRESSION IN HUMAN MONONUCLEAR CELLS By Monika D. Ruchała, M.S. A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science at Virginia Commonwealth University. Virginia Commonwealth University, 2014. Director: Dr. James P. Bennett Jr, M.D., Ph.D., Bemiss Professor Departments of Neurology, Psychiatry and Physiology and Biophysics Adult neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS), have been intensively studied in recent years in pursuit of mechanisms responsible for origin and progression. One emerging theme is mitochondrial energetic deficiency as a mechanism of neuronal death. Recent descriptions of protocols to generate induced pluripotent stems cells (iPSCs) from living patients offer the potential to create unique disease models. This model can potentially lead to crucial advances in developing treatment options for a wide variety of neurodegenerative diseases. In this thesis, we attempt to induce iPSCs from mononuclear cells (MNC) in peripheral blood acquired from patients with ALS and healthy control (CTL) subjects, and analyze their mitochondrial genomes. The reprogramming of MNC to yield iPSC was done by nucleofection of an episomal plasmid pEB­ C5, expressing OriP sequences of the Epstein­Barr and five reprogramming transgenes Oct4, Sox2, Klf4, c­Myc and Lin28. We investigated the expression of mitochondrial DNA genes, ND2, ND4, COXIII and 12s rRNA in the ALS and CTL MNC before and after their culturing. The results implicate deregulated mitochondrial bioenergetics as a characteristic of ALS. Future work will establish whether these abnormalities in mitochondrial bioenergetics persist in iPSC’s and iPSC-derived neurons from ALS subject
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Zainuddin, Zafarina. "The analysis of human mitochondrial DNA in peninsular Malaysia." Thesis, University of Glasgow, 2004. http://theses.gla.ac.uk/4520/.

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Mitochondrial DNA analysis was undertaken on samples collected from two populations in Peninsular Malaysia, the Modern Malay (102 samples) and Orang Asli (59 samples from Jahai and Kinsiu sub-groups). The hypervariable region 1 (HV1) of the mtDNA control region was amplified and sequenced. Polymorphisms were reported by aligning each sequence to the Cambridge Reference Sequence (CRS). A total of 94 polymorphisms were observed in the Modern Malay samples, which formed 75 different haplotypes. The Orang Asli showed notably lower number of the HV1 region variations, with only 28 polymorphisms and 13 haplotypes observed. Genetic diversity calculated for the Modern Malays and Orang Asli were 0.989 and 0.818, respectively. Probability of random match calculated was 0.0202 for the Modern Malays and 0.1962 for the Orang Asli. The mtDNA coding region variations was examined using RFLP analysis. Combination of both RFLP and HV1 sequence data had placed the Modern Malays into three major Southeast Asian haplogroups, M, B and F. These findings had initially suggested that the Modern Malays shared a common lineage with other populations within this region. Two novel sub-clusters, M21a and R21 were found at a high frequency within the Orang Asli samples. These sub-clusters, which have also been found in other Semang sub-groups appear to be indigenous Semang haplogroups. The limited number of mtDNA haplotypes shared between the Modern Malays and Orang Asli suggested discontinuity of mtDNA between these populations. Even though both populations were believed to be among the earliest populations of Peninsular Malaysia, this result indicates that the Modern Malays were not direct descendants of the Orang Asli. Minisequencing analysis was carried for further interrogation of the mtDNA coding region polymorphisms. Besides mtDNA analysis, the autosomal STR markers were also examined using PowerPlex® 16 system for both populations. These data could provide more information when added to the available STR database for Malaysian populations.
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He, Langping. "Role of mitochondrial DNA mutation in ageing and disease." Thesis, University of Newcastle Upon Tyne, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251942.

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Balinang, Joyce. "The Regulation of Mitochondrial DNMT1 During Oxidative Stress." VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/2826.

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Epigenetics is the study of heritable gene expression due to alterations in the DNA structure other than the underlying DNA sequence. DNA methylation is one of the three types of epigenetic modifications found in the eukaryotic system. It involves the incorporation of a methyl group at the 5-position of cytosine residues in the DNA. DNA methylation is associated with several notorious disorders and diseases including Fragile X Syndrome, neurodegenerative disease (Parkinson’s, Alzhiemer, etc), diabetes and cancer. Cytosine methylation of mitochondrial DNA (mtDNA) was first demonstrated several decades ago but the mechanism of generating cytosine modification and its functional importance remain elusive. Our laboratory recently demonstrated that the enzyme involved in cytosine modification of mtDNA is a novel mitochondrial isoform of DNA Methyltransferase 1, mtDNMT1. This protein is encoded in the nucleus and targeted to the mitochondria via a N-terminal targeting sequence. Bioinformatic analysis of the DNMT1 coding sequence showed a consensus NRF1 binding site that coincidently overlaps a p53 binding site within the promoter region, previously shown by this group to repress DNMT1 expression. Previous studies in the Taylor laboratory showed that mtDNMT protein expression was regulated by the transcription factor NRF1 as well as its coactivator PGC1α. PGC1α and NRF1 stimulate a large body of genes that are involved in mitochondrial biogenesis and cellular respiration in response to environmental stress. Considering the previous findings in our laboratory regarding mtDNMT1 regulation and the importance of PGC1α and NRF1 in oxidative homeostasis, we asked whether there is a mitochondrial epigenetic component in the cell’s response to cellular stress and whether up-regulation of mtDNMT1 might be part of the general response to this stress. To investigate the relationship between mtDNA methylation and oxidative homeostasis we examined the regulation of mtDNMT1 by transcription factors that respond to oxidative stress. Conditions that induced oxidative stress were applied to HCT 116 and SH-SY5Y cell lines and the protein expression of DNMT1 was observed. Ethanol and hypoxia- induced oxidative stress were observed to increase to protein level of mtDNMT1 while total DNMT1 level either remained constant or decreased. The protein level of PGC1α and NRF1 remained low in HCT 116 cells exposed to hypoxic stress, despite elevated mtDNMT1 protein level. ChIP analysis of HCT 116 cells exposed to hypoxic stress demonstrated that NRF1 and PGC1α are not regulating the transcription of DNMT1i in the mitochondria. However, we observed that p53 dissociated from the DNMT1 promoter upon hypoxic stress, indicating that the up-regulation of mtDNMT1 is through the relief of p53 suppression. The findings of this investigation proved that mtDNMT1 is receptive to oxidative stress through the regulation by p53 and suggested that mitochondrial epigenetics may be playing an integral role in the cellular stress response toward hypoxia.
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Books on the topic "Mitochondrial medicine"

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Weissig, Volkmar, and Marvin Edeas, eds. Mitochondrial Medicine. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1266-8.

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Weissig, Volkmar, and Marvin Edeas, eds. Mitochondrial Medicine. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1270-5.

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Weissig, Volkmar, and Marvin Edeas, eds. Mitochondrial Medicine. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1262-0.

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Weissig, Volkmar, and Marvin Edeas, eds. Mitochondrial Medicine. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2257-4.

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Weissig, Volkmar, and Marvin Edeas, eds. Mitochondrial Medicine. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2288-8.

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Gvozdjáková, Anna, ed. Mitochondrial Medicine. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6714-3.

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S, DiMauro, Hirano Michio, and Schon Eric A, eds. Mitochondrial medicine. Abingdon [U.K.]: Informa Healthcare, 2006.

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Mitochondrial medicine. New York: Humana Press, 2015.

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Advances in mitochondrial medicine. Dordrecht: Springer Verlag, 2012.

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Scatena, Roberto, Patrizia Bottoni, and Bruno Giardina, eds. Advances in Mitochondrial Medicine. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-2869-1.

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Book chapters on the topic "Mitochondrial medicine"

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Gvozdjáková, Anna. "Mitochondrial Medicine." In Mitochondrial Medicine, 103–13. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6714-3_5.

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Rodenburg, Richard J. T., and Jan A. M. Smeitink. "Mitochondrial Medicine." In Chemical Biology, 445–60. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118435762.ch22.

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Gvozdjáková, Anna, Anna Hlavatá, Jarmila Kucharská, Patrik Palacka, and Ján Murín. "Coenzyme Q10 Supplementation in Clinical Medicine." In Mitochondrial Medicine, 323–33. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6714-3_17.

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Gvozdjáková, Anna, Jaromír Horecký, Ol'ga Vančová, Jarmila Kucharská, Katarína Bauerová, and Silvester Poništ. "Coenzyme Q10 Supplementation in Experimental Medicine." In Mitochondrial Medicine, 335–42. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6714-3_18.

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Gvozdjáková, Anna. "Mitochondrial Physiology." In Mitochondrial Medicine, 1–17. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6714-3_1.

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Gazdík, František, and Katarína Gazdíková. "Mitochondrial Immunology." In Mitochondrial Medicine, 247–62. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6714-3_12.

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Gvozdjáková, Anna. "Mitochondrial “Spermatopathy”." In Mitochondrial Medicine, 263–66. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6714-3_13.

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Pecháň, Ivan. "Mitochondrial Cardiology." In Mitochondrial Medicine, 115–24. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6714-3_6.

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Čársky, Jozef, Anna Gvozdjáková, Miroslav Mikulecký, Jarmila Kucharská, and Ram B. Singh. "Mitochondrial Diabetology." In Mitochondrial Medicine, 129–60. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6714-3_8.

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Gazdíková, Katarína, and František Gazdík. "Mitochondrial Nephrology." In Mitochondrial Medicine, 161–87. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6714-3_9.

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Conference papers on the topic "Mitochondrial medicine"

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Fang Shen, Li-ping Wu, Yuan Lu, Hua-wei Liang, I. C. Bruce, and Qiang Xia. "Mitochondrial Permeability Transition Dynamics: An Indicator of Mitochondrial Potassium Channel Opener." In 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1616201.

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Krestinin, Roman, Yulia Baburina, Irina Odinokova, Linda Sotnikova, and Olga Krestinina. "ASTAXANTHIN REDUCES ISOPROTERINOL-INDUCED MITOCHONDRIAL DYSFUNCTION." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2183.sudak.ns2021-17/212-213.

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Tsomartova, Dibakhan, Nataliya Yaglova, Sergey Obernikhin, Svetlana Nazimova, and Valentin Vasilyevich Yaglov. "ALTERED CYTOPHYSIOLOGY OF EPINEPHRINE-PRODUCING CELLS IN RATS AFTER CHRONIC EXPOSURE TO LOW DOSES OF DDT." In NEW TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2021. http://dx.doi.org/10.47501/978-5-6044060-1-4.12.

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Chronic low-dose exposure to dichlorodiphenyltrichloroethane does not diminish epinephrine production since epinephrine-secreting adrenal cells significantly intensify mitochondrial ac-tivity to restore epinephrine secretion.
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Pieczara, Anna, Ewelina Matuszyk, and Malgorzata Baranska. "Mitochondrial activity studied by Raman spectroscopy." In Advanced Chemical Microscopy for Life Science and Translational Medicine 2022, edited by Garth J. Simpson, Ji-Xin Cheng, and Wei Min. SPIE, 2022. http://dx.doi.org/10.1117/12.2608819.

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bhatt, shruti, david weinstock, and Anthony Letai. "Abstract 418: Mitochondrial perturbations as a novel approach to personalized medicine." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-418.

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Horvath, Rita. "Mitochondrial Diseases: Diagnosis and Novel Approach for Treatment." In Congenital Dystrophies - Neuromuscular Disorders Precision Medicine: Genomics to Care and Cure. Hamad bin Khalifa University Press (HBKU Press), 2020. http://dx.doi.org/10.5339/qproc.2020.nmd.18.

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Vernier, P. Thomas. "Mitochondrial membrane permeabilization with nanosecond electric pulses." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6090169.

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Cortassa, S., M. A. Aon, B. O'Rourke, and R. L. Winslow. "Metabolic control analysis applied to mitochondrial networks." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6091157.

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Wang, Erkang, Jesse Wilson, Adam J. Chicco, and Luke A. whitcomb. "Transient absorption imaging of mitochondrial redox in muscle fibers." In Advanced Chemical Microscopy for Life Science and Translational Medicine 2022, edited by Garth J. Simpson, Ji-Xin Cheng, and Wei Min. SPIE, 2022. http://dx.doi.org/10.1117/12.2608844.

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AVRAHAM, MAYEVSKY. "SHEDDING LIGHT ON LIFE: OPTICAL ASSESSMENT OF MITOCHONDRIAL FUNCTION AND TISSUE VITALITY IN BIOLOGY AND MEDICINE." In Proceedings of the 6th International Conference on Photonics and Imaging in Biology and Medicine (PIBM 2007). WORLD SCIENTIFIC, 2008. http://dx.doi.org/10.1142/9789812832344_0001.

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