Relevant bibliographies by topics / Mitochondria, mitochondrial diseases, Opa1, therapies

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters

Academic literature on the topic 'Mitochondria, mitochondrial diseases, Opa1, therapies'

Author: Grafiati
Published: 9 March 2023
Last updated: 28 July 2025

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Journal articles on the topic "Mitochondria, mitochondrial diseases, Opa1, therapies"

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Xia, Yi, Xu Zhang, Peng An, Junjie Luo, and Yongting Luo. "Mitochondrial Homeostasis in VSMCs as a Central Hub in Vascular Remodeling." International Journal of Molecular Sciences 24, no. 4 (2023): 3483. http://dx.doi.org/10.3390/ijms24043483.

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Vascular remodeling is a common pathological hallmark of many cardiovascular diseases. Vascular smooth muscle cells (VSMCs) are the predominant cell type lining the tunica media and play a crucial role in maintaining aortic morphology, integrity, contraction and elasticity. Their abnormal proliferation, migration, apoptosis and other activities are tightly associated with a spectrum of structural and functional alterations in blood vessels. Emerging evidence suggests that mitochondria, the energy center of VSMCs, participate in vascular remodeling through multiple mechanisms. For example, pero
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Samant, Sadhana A., Hannah J. Zhang, Zhigang Hong, et al. "SIRT3 Deacetylates and Activates OPA1 To Regulate Mitochondrial Dynamics during Stress." Molecular and Cellular Biology 34, no. 5 (2013): 807–19. http://dx.doi.org/10.1128/mcb.01483-13.

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Mitochondrial morphology is regulated by the balance between two counteracting mitochondrial processes of fusion and fission. There is significant evidence suggesting a stringent association between morphology and bioenergetics of mitochondria. Morphological alterations in mitochondria are linked to several pathological disorders, including cardiovascular diseases. The consequences of stress-induced acetylation of mitochondrial proteins on the organelle morphology remain largely unexplored. Here we report that OPA1, a mitochondrial fusion protein, was hyperacetylated in hearts under pathologic
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Ranieri, Michela, Simona Brajkovic, Giulietta Riboldi, et al. "Mitochondrial Fusion Proteins and Human Diseases." Neurology Research International 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/293893.

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Mitochondria are highly dynamic, complex organelles that continuously alter their shape, ranging between two opposite processes, fission and fusion, in response to several stimuli and the metabolic demands of the cell. Alterations in mitochondrial dynamics due to mutations in proteins involved in the fusion-fission machinery represent an important pathogenic mechanism of human diseases. The most relevant proteins involved in the mitochondrial fusion process are three GTPase dynamin-like proteins: mitofusin 1 (MFN1) and 2 (MFN2), located in the outer mitochondrial membrane, and optic atrophy pr
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Tokuyama, Takeshi, and Shigeru Yanagi. "Role of Mitochondrial Dynamics in Heart Diseases." Genes 14, no. 10 (2023): 1876. http://dx.doi.org/10.3390/genes14101876.

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Mitochondrial dynamics, including fission and fusion processes, are essential for heart health. Mitochondria, the powerhouses of cells, maintain their integrity through continuous cycles of biogenesis, fission, fusion, and degradation. Mitochondria are relatively immobile in the adult heart, but their morphological changes due to mitochondrial morphology factors are critical for cellular functions such as energy production, organelle integrity, and stress response. Mitochondrial fusion proteins, particularly Mfn1/2 and Opa1, play multiple roles beyond their pro-fusion effects, such as endoplas
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Toda, Yuki, Sang-Bing Ong, Toshiyuki Yano, et al. "Downregulation of Mitochondrial Fusion Protein Expression Affords Protection from Canonical Necroptosis in H9c2 Cardiomyoblasts." International Journal of Molecular Sciences 25, no. 5 (2024): 2905. http://dx.doi.org/10.3390/ijms25052905.

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Necroptosis, a form of necrosis, and alterations in mitochondrial dynamics, a coordinated process of mitochondrial fission and fusion, have been implicated in the pathogenesis of cardiovascular diseases. This study aimed to determine the role of mitochondrial morphology in canonical necroptosis induced by a combination of TNFα and zVAD (TNF/zVAD) in H9c2 cells, rat cardiomyoblasts. Time-course analyses of mitochondrial morphology showed that mitochondria were initially shortened after the addition of TNF/zVAD and then their length was restored, and the proportion of cells with elongated mitoch
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Wu, Bangwei, Jian Li, Huanchun Ni, et al. "TLR4 Activation Promotes the Progression of Experimental Autoimmune Myocarditis to Dilated Cardiomyopathy by Inducing Mitochondrial Dynamic Imbalance." Oxidative Medicine and Cellular Longevity 2018 (June 26, 2018): 1–15. http://dx.doi.org/10.1155/2018/3181278.

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Mitochondrial dynamic imbalance associates with several cardiovascular diseases. However, the role of mitochondrial dynamics in TLR4 activation-mediated dilated cardiomyopathy (DCM) progress remains unknown. A model of experimental autoimmune myocarditis (EAM) was established in BALB/c mice on which TLR4 activation by LPS-EB or TLR4 inhibition by LPS-RS was performed to induce chronic inflammation for 5 weeks. TLR4 activation promoted the transition of EAM to DCM as demonstrated by increased cardiomyocyte apoptosis, myocardial fibrosis, ventricular dilatation, and declined heart function. TLR4
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Schuettpelz, Jana, Alexandre Janer, Hana Antonicka, and Eric A. Shoubridge. "The role of the mitochondrial outer membrane protein SLC25A46 in mitochondrial fission and fusion." Life Science Alliance 6, no. 6 (2023): e202301914. http://dx.doi.org/10.26508/lsa.202301914.

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Mutations inSLC25A46underlie a wide spectrum of neurodegenerative diseases associated with alterations in mitochondrial morphology. We established an SLC25A46 knock-out cell line in human fibroblasts and studied the pathogenicity of three variants (p.T142I, p.R257Q, and p.E335D). Mitochondria were fragmented in the knock-out cell line and hyperfused in all pathogenic variants. The loss of SLC25A46 led to abnormalities in the mitochondrial cristae ultrastructure that were not rescued by the expression of the variants. SLC25A46 was present in discrete puncta at mitochondrial branch points and ti
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Suárez-Rivero, Juan M., Juan López-Pérez, Inés Muela-Zarzuela, et al. "Neurodegeneration, Mitochondria, and Antibiotics." Metabolites 13, no. 3 (2023): 416. http://dx.doi.org/10.3390/metabo13030416.

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Neurodegenerative diseases are characterized by the progressive loss of neurons, synapses, dendrites, and myelin in the central and/or peripheral nervous system. Actual therapeutic options for patients are scarce and merely palliative. Although they affect millions of patients worldwide, the molecular mechanisms underlying these conditions remain unclear. Mitochondrial dysfunction is generally found in neurodegenerative diseases and is believed to be involved in the pathomechanisms of these disorders. Therefore, therapies aiming to improve mitochondrial function are promising approaches for ne
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Carelli, Valerio, Chiara La Morgia, Luisa Iommarini, et al. "Mitochondrial Optic Neuropathies: How Two Genomes may Kill the Same Cell Type?" Bioscience Reports 27, no. 1-3 (2007): 173–84. http://dx.doi.org/10.1007/s10540-007-9045-0.

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Ocular involvement is a prevalent feature in mitochondrial diseases. Leber's hereditary optic neuropathy (LHON) and dominant optic atrophy (DOA) are both non-syndromic optic neuropathies with a mitochondrial etiology. LHON is associated with point mutations in the mitochondrial DNA (mtDNA), which affect subunit genes of complex I. The majority of DOA patients harbor mutations in the nuclear-encoded protein OPA1, which is targeted to mitochondria and participates to cristae organization and mitochondrial network dynamics. In both disorders the retinal ganglion cells (RGCs) are specific cellular
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Liesa, Marc, Manuel Palacín, and Antonio Zorzano. "Mitochondrial Dynamics in Mammalian Health and Disease." Physiological Reviews 89, no. 3 (2009): 799–845. http://dx.doi.org/10.1152/physrev.00030.2008.

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The meaning of the word mitochondrion (from the Greek mitos, meaning thread, and chondros, grain) illustrates that the heterogeneity of mitochondrial morphology has been known since the first descriptions of this organelle. Such a heterogeneous morphology is explained by the dynamic nature of mitochondria. Mitochondrial dynamics is a concept that includes the movement of mitochondria along the cytoskeleton, the regulation of mitochondrial architecture (morphology and distribution), and connectivity mediated by tethering and fusion/fission events. The relevance of these events in mitochondrial
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Dissertations / Theses on the topic "Mitochondria, mitochondrial diseases, Opa1, therapies"

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CIVILETTO, GABRIELE. "Opa1 overexpression as potential therapy in mitochondrial diseases." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2014. http://hdl.handle.net/10281/55460.

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Mitochondrial disorders are a group of highly invalidating human conditions due to defective oxidative phosphorylation, for which no effective treatment is nowadays available. In order to develop effective therapies for these disorders, I focused on an experimental approach based on the manipulation of mitochondrial morphology. Opa1 is a GTPase of the inner mitochondrial membrane involved in both mitochondrial fusion and cristae shaping. The role of OPA1 in mitodynamics has also a documented impact on controlling the assembly of the respiratory supercomplexes and respiratory proficiency. Base
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Book chapters on the topic "Mitochondria, mitochondrial diseases, Opa1, therapies"

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Malhotra, Ashim, and Shivani Soni. "Examining the Effect of Mitochondrial Fission and Fusion Events on the Heart." In Emerging Applications, Perspectives, and Discoveries in Cardiovascular Research. IGI Global, 2017. http://dx.doi.org/10.4018/978-1-5225-2092-4.ch005.

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Mitochondria constitute an integral structural and functional part of the cardiac muscle. The heart muscle relies on the mitochondrial production of fatty acids and ATP as sources of energy during different stages of human growth and development. New mitochondria are created from existing ones by a process called mitochondrial biogenesis which involves both fusion and fission events controlled by a bevy of proteins such as Drp1, OPA1, Mfn1, and Mfn2. In this chapter, we examine the role of these mitochondrial fission and fusion proteins in regulating various heart diseases, particularly, reper
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Basavalingiah, Anish J., Shi Fang Yan, and Shirley ShiDu Yan. "Mitochondria Are a Potential Therapeutic Target for Alzheimer’s Disease." In The Oxford Handbook of Mitochondria. Oxford University Press, 2023. http://dx.doi.org/10.1093/oxfordhb/9780190932183.013.23.

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Abstract Mitochondria are organelles that play an essential role in many cellular processes including, but not limited to, oxidative phosphorylation, calcium homeostasis, and apoptosis signaling. Mitochondrial dysfunction is pertinent to the pathology of several neurodegenerative diseases; more specifically, it has been shown to be involved in Alzheimer’s Disease (AD). Moreover, mitochondrial dysfunction in AD manifests through various mechanisms, including opening of mitochondrial permeability transition pore (mPTP), impaired mitochondrial dynamics, dysfunction of mitophagy, and aberrant prot
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Verma, Manish Kumar. "Natural Products Modulating Mitophagy Implications for Cancer Therapy." In Roles of Mitophagy in Cancer Regulation. IGI Global, 2025. https://doi.org/10.4018/979-8-3693-3836-0.ch010.

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Mitochondrial dysfunction is a hallmark of cancer, contributing to tumorigenesis, and therapeutic resistance. Mitophagy, the selective removal of damaged or dysfunctional mitochondria, plays a crucial role in maintaining cellular homeostasis and preventing the accumulation of cellular stress. The dysregulation of mitophagy in cancer often leads to the accumulation of damaged mitochondria, promoting tumorigenesis and hampering the efficacy of conventional therapies. Natural products like polyphenols, flavonoids, alkaloids, terpenoids influencing mitophagy, through AMP-activated protein kinase (
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