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- W2480572321 abstract "The highly regulated processes of mitochondrial fusion, fission (division), and trafficking, collectively called mitochondrial dynamics, determine the cell-type specific morphology, intracellular distribution, and activity of these critical organelles. These processes modulate a variety of mitochondrial functions, allowing living cells to respond properly to frequently changing environmental conditions. The tightly controlled balance between fusion and fission is of utmost importance in the highly energy demanding cells, such as cardiac and skeletal muscles and neuronal cells. A shift towards fission leads to mitochondrial fragmentation, whereas a shift towards fusion results in the formation of the large mitochondrial networks. Large dynamin-related Mfn1, Mfn2, and OPA1 constitute the core machinery promoting mitochondrial fusion. Mfn1 and Mfn2, localized on the mitochondrial outer membrane (MOM), mediate MOM fusion, whereas OPA1, located in the mitochondrial inner membrane (MIM), promotes fusion of the MIM as well as cristae remodeling. A dynamin-related Drp1 along with Fis1 and Mff are the core components of mitochondrial fission machinery in mammalian cells. All known core mammalian fission proteins are localized in the MOM, but it is very little known about MIM fission. Currently, the most characterized defects in components involved in mitochondrial dynamics have been found in inherited neurological and neurodegenerative disorders. Although intracellular architecture of mature cardiomyocytes greatly restricts mitochondrial dynamics, this process occurs in the heart, albeit much slower than in other cell types. Emerging evidence strongly suggests that impairment of mitochondrial dynamics causes mitochondrial dysfunction and can contribute to the pathogenesis of various cardiovascular diseases (CVDs), including ischemia-reperfusion injury (IRI), various cariomyopathies, and heart failure (HF). Pharmacological targeting components of the mitochondrial fusion and fission machineries to normalize normal mitochondrial numbers, morphology, and function may be a novel therapeutic modality for CVD treatment. Despite significant progress in our understanding of the molecular mechanisms of mitochondrial dynamics in the heart, further extensive research is needed to translate this knowledge into the development of efficient therapies for CVD." @default.
- W2480572321 created "2016-08-23" @default.
- W2480572321 creator A5022739391 @default.
- W2480572321 date "2014-01-01" @default.
- W2480572321 modified "2023-09-24" @default.
- W2480572321 title "The Emerging Role of Mitochondrial Dynamics in Cardiovascular Disease" @default.
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