We are analyzing https://link.springer.com/article/10.1007/s00395-016-0578-x.

Title:
Inhibition of mitochondrial fission as a molecular target for cardioprotection: critical importance of the timing of treatment | Basic Research in Cardiology
Description:
Recent attention has focused on the concept that mitochondrial dynamics—that is, the balance between mitochondrial fusion and fission (fragmentation)—may play a pivotal role in determining cell fate in the setting of myocardial ischemia–reperfusion injury. In this regard, there is an emerging consensus that: (1) ischemia–reperfusion favors mitochondrial fragmentation and (2) strategies aimed at inhibiting the translocation of dynamin-related protein 1 (DRP1: the ‘master regulator’ of fission) from the cytosol to the mitochondria, when initiated as a pretreatment, are cardioprotective. However, direct molecular evidence of a cause-and-effect relationship between mitochondrial fission and cardiomyocyte death has not been established. To address this issue, we used a well-characterized in vitro, immortal cultured cardiomyocyte model to establish whether subcellular redistribution of DRP1 to mitochondria: (1) is triggered by hypoxia–reoxygenation; (2) plays a causal role in hypoxia–reoxygenation-induced cytochrome c release (harbinger of apoptosis) and cardiomyocyte death; and (3) represents a molecular mechanism that can be targeted in a clinically relevant time frame to render cells resistant to lethal hypoxia–reoxygenation injury. Our results provide direct evidence that the redistribution of DRP1 to mitochondria contributes to cardiomyocyte death, and corroborate the previous observations that the pre-ischemic inhibition of DRP1 translocation is cardioprotective. Moreover, we report the novel finding that—in marked contrast to the data obtained with pretreatment—inhibition of DRP1 translocation initiated at the time of reoxygenation had complex, unexpected and unfavorable consequences: i.e., attenuated cardiomyocyte apoptosis but exacerbated total cell death, possibly via concurrent upregulation of necroptosis.
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Keywords {🔍}

pubmed, article, google, scholar, mitochondrial, cas, cell, fission, death, central, injury, drp, przyklenk, ischemiareperfusion, apoptosis, mol, dong, fusion, role, protein, cardiomyocyte, biol, rev, nat, research, inhibition, myocardial, dynamics, usa, state, medicine, privacy, cookies, content, data, karin, dynaminrelated, heart, permeability, transition, kinase, yuan, cardiac, embo, wang, function, publish, search, basic, molecular,

Topics {✒️}

month download article/chapter myocardial ischemia–reperfusion injury lethal hypoxia–reoxygenation injury brain ischemia/reperfusion injury hypoxia–reoxygenation-induced cytochrome dynamin-related protein 1 dynamin-related protein-1 ca2+-induced permeability transition drp1-dependent mitochondrial fission article basic research archer sl ischemia–reperfusion injury ischemia/reperfusion injury full article pdf mitochondrial dynamics—mitochondrial fission cultured hl-1 cardiomyocytes global cerebral ischemia related subjects acute myocardial infarction privacy choices/manage cookies mitochondrial permeability transition smith cc claycomb wc fission proteins mediated diastolic dysfunction radical induced depolarization excessive mitochondrial fission reduce mitochondrial fission attenuated cardiomyocyte apoptosis hypoxia–reoxygenation determining cell fate enhancing macroautophagy protects senp3-mediated desumoylation article dong direct molecular evidence drp1/fis1 availability disease article 06 article log european economic area lanson na jr izzo nj jr retains phenotypic characteristics quantifying western blots rip1 kinase signalling mitochondrial quality control hl-1 cells treating cardiovascular disease article number 59 conditions privacy policy render cells resistant

Questions {❓}

Martinou JC, Youle RJ (2006) Which came first, the cytochrome c release or the mitochondrial fission?
Smith CC, Davidson SM, Lim SY, Simpkin JC, Hothersall JS, Yellon DM (2007) Necrostatin: a potentially novel cardioprotective agent?

Schema {🗺️}

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