We are analyzing https://link.springer.com/article/10.1007/s10741-016-9530-2.

Title:
Mitochondrial dynamics and cell death in heart failure | Heart Failure Reviews
Description:
The highly regulated processes of mitochondrial fusion (joining), fission (division) and trafficking, collectively called mitochondrial dynamics, determine cell-type specific morphology, intracellular distribution and activity of these critical organelles. Mitochondria are critical for cardiac function, while their structural and functional abnormalities contribute to several common cardiovascular diseases, including heart failure (HF). The tightly balanced mitochondrial fusion and fission determine number, morphology and activity of these multifunctional organelles. Although the intracellular architecture of mature cardiomyocytes greatly restricts mitochondrial dynamics, this process occurs in the adult human heart. Fusion and fission modulate multiple mitochondrial functions, ranging from energy and reactive oxygen species production to Ca2+ homeostasis and cell death, allowing the heart to respond properly to body demands. Tightly controlled balance between fusion and fission is of utmost importance in the high energy-demanding cardiomyocytes. A shift toward fission leads to mitochondrial fragmentation, while a shift toward fusion results in the formation of enlarged mitochondria and in the fusion of damaged mitochondria with healthy organelles. Mfn1, Mfn2 and OPA1 constitute the core machinery promoting mitochondrial fusion, whereas Drp1, Fis1, Mff and MiD49/51 are the core components of fission machinery. Growing evidence suggests that fusion/fission factors in adult cardiomyocytes play essential noncanonical roles in cardiac development, Ca2+ signaling, mitochondrial quality control and cell death. Impairment of this complex circuit causes cardiomyocyte dysfunction and death contributing to heart injury culminating in HF. Pharmacological targeting of components of this intricate network may be a novel therapeutic modality for HF treatment.
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28 years and 1 months (reg. 1997-05-29).

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Keywords {🔍}

pubmed, article, google, scholar, cas, mitochondrial, central, cell, biol, fission, fusion, heart, mitochondria, protein, mol, drp, res, death, cardiac, opa, mitofusin, dynamics, mitophagy, chen, chem, function, membrane, disease, apoptosis, autophagy, mammalian, nat, circ, dynaminrelated, failure, morphology, biophys, med, dorn, sci, wang, parkin, regulation, biochim, acta, physiol, youle, cells, embo, usa,

Topics {✒️}

increased o-linked-beta-n-acetylglucosamine modification parkin-ubiquitin-p62-mediated mitochondrial priming month download article/chapter dorn gw 2nd dynamin-related protein drp1 x-linked vacuolar cardiomyopathy bax/bak promote sumoylation mitochondrial dynamin-related protein article marín-garcía dimeric dnm1-g385d interacts bax/bak-dependent release pgc1alpha-mediated mitofusin-2 deficiency mitochondrial fission-stimulating protein pro-fission mitochondrial protein metalloprotease-mediated opa1 processing m-aaa protease isoenzymes multi-step process requiring pink1/parkin-mediated mitophagy opa1-dependent cristae remodeling cardiac-expressed death factors pink1/parkin-dependent manner endoplasmic reticulum-mitochondria crosstalk josé marín-garcía full article pdf dynamin-related protein 1 dynamin-related protein-1 stress-induced permeability transition high energy-demanding cardiomyocytes heart failure published ros-induced mitochondrial dysfunction stress-induced mitochondrial hyperfusion mitochondrial dynamics—mitochondrial fission mitochondrial outer membrane martins de brito chang cr hoppel cl postnatal metabolic remodeling primary mitophagic cardiomyopathy privacy choices/manage cookies mitochondrial membrane fusion membrane remodeling induced ribeiro rf jr narendra dp membrane fission catalyst cardiac oxygen sensors pink1/parkin pathway fusion/fission factors pancreatic beta-cell adult human heart transmembrane gtpase fzo

Questions {❓}

Martinou JC, Youle RJ (2006) Which came first, the cytochrome c release or the mitochondrial fission?
Ziviani E, Whitworth AJ (2010) How could Parkin-mediated ubiquitination of mitofusin promote mitophagy?

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         description:The highly regulated processes of mitochondrial fusion (joining), fission (division) and trafficking, collectively called mitochondrial dynamics, determine cell-type specific morphology, intracellular distribution and activity of these critical organelles. Mitochondria are critical for cardiac function, while their structural and functional abnormalities contribute to several common cardiovascular diseases, including heart failure (HF). The tightly balanced mitochondrial fusion and fission determine number, morphology and activity of these multifunctional organelles. Although the intracellular architecture of mature cardiomyocytes greatly restricts mitochondrial dynamics, this process occurs in the adult human heart. Fusion and fission modulate multiple mitochondrial functions, ranging from energy and reactive oxygen species production to Ca2+ homeostasis and cell death, allowing the heart to respond properly to body demands. Tightly controlled balance between fusion and fission is of utmost importance in the high energy-demanding cardiomyocytes. A shift toward fission leads to mitochondrial fragmentation, while a shift toward fusion results in the formation of enlarged mitochondria and in the fusion of damaged mitochondria with healthy organelles. Mfn1, Mfn2 and OPA1 constitute the core machinery promoting mitochondrial fusion, whereas Drp1, Fis1, Mff and MiD49/51 are the core components of fission machinery. Growing evidence suggests that fusion/fission factors in adult cardiomyocytes play essential noncanonical roles in cardiac development, Ca2+ signaling, mitochondrial quality control and cell death. Impairment of this complex circuit causes cardiomyocyte dysfunction and death contributing to heart injury culminating in HF. Pharmacological targeting of components of this intricate network may be a novel therapeutic modality for HF treatment.
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