We are analyzing https://link.springer.com/article/10.1007/s10495-008-0296-4.

Title:
The cardioprotective effect of postconditioning is mediated by ARC through inhibiting mitochondrial apoptotic pathway | Apoptosis
Description:
Postconditioning protects the heart against ischemia/reperfusion injury by inhibiting cardiomyocyte apoptosis. However, the molecular mechanism by which postconditioning suppresses apoptosis remains to be fully understood. Apoptosis repressor with caspase recruitment domain (ARC) has been demonstrated to possess the ability to protect cardiomyocytes from apoptosis induced by ischemia/reperfusion. It is not yet clear as to whether ARC contributes to the inhibitory effect of postconditioning against cardiomyocyte apoptosis. The cultured cardiomyocytes from 1-day old male Sprague–Dawley rats were exposed to 3 h hypoxia followed by 3 h of reoxygenation. Cells were postconditioned by three cycles each of 5 min reoxygenation and 5 min hypoxia before 3 h of reoxygenation. Hypoxia/reoxygenation led to a decrease of endogenous ARC protein levels. In contrast, postconditioning could block the reduction of endogenous ARC protein levels. Interestingly, inhibition of endogenous ARC expression by ARC antisense oligodeoxynucleotides reduced the inhibitory effect of postconditioning against apoptosis. Furthermore, our data showed that postconditioning suppressed the loss of mitochondrial membrane potential, Bax activation and the release of mitochondrial cytochrome c to cytosol. However, these inhibitory effects of postconditioning disappeared upon knockdown of endogenous ARC. Our data for the first time demonstrate that ARC plays an essential role in mediating the cardioprotective effect of postconditioning against apoptosis initiated by the mitochondrial pathway.
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Keywords {🔍}

article, google, scholar, apoptosis, pubmed, cas, arc, postconditioning, cell, mitochondrial, death, biol, caspase, repressor, recruitment, domain, protein, myocardial, effect, injury, cardiomyocyte, role, reperfusion, res, privacy, cookies, content, data, inhibiting, pathway, heart, ischemiareperfusion, inhibition, publish, research, search, cardioprotective, apoptotic, liu, protects, cardiomyocytes, inhibitory, reoxygenation, endogenous, access, preconditioning, physiol, circ, pathways, dois,

Topics {✒️}

month download article/chapter xinlan ge & xiuhua liu male sprague–dawley rats nonhomotypic death-fold interactions ischemia/hypoxic cel death bid-induced conformational change myocardial ischemia/reperfusion injury myocardial ischemia–reperfusion injury phosphatidylinositol 3-kinase-akt pathway heart-derived h9c2 cells full article pdf apoptotic cell death article apoptosis aims privacy choices/manage cookies ischemia/reperfusion injury intrinsic death pathways ischemia induced activation hypoxic postconditioning enhances tat protein transduction antiapoptotic protein arc related subjects isolated perfused hearts article li preconditioned rabbit heart inhibiting ros generation inhibiting cardiomyocyte apoptosis �modified reperfusion” protects sun hy hypoxia-induced apoptosis basic medical science endogenous arc expression caspase recruitment domain european economic area double-edged sword intracellular ca2+ overload peroxynitrite formation reliable fluorescent probe assess delta psi arc mediates regulation p53 initiates apoptosis conditions privacy policy arc inhibits cytochrome mitochondrial membrane potential preserving mitochondrial function proteins-essential initiators article log accepting optional cookies tat-apoptosis repressor author information authors mitochondrial pathway

Questions {❓}

Braunwald E, Kloner RA (1985) Myocardial reperfusion: a double-edged sword?

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