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Inhibition of myocardial reperfusion injury by ischemic postconditioning requires sirtuin 3-mediated deacetylation of cyclophilin D

机译:缺血后适应抑制心肌再灌注损伤需要Sirtuin 3介导的亲环蛋白D脱乙酰化

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摘要

Rationale. How ischemic postconditioning can inhibit opening of the mitochondrial permeability transition pore (PTP) and subsequent cardiac myocytes death at reperfusion remains unknown. Recent studies have suggested that de-acetylation of cyclophilin D (CyPD) by sirtuin 3 (SIRT3) can modulate its binding to the PIP.
机译:基本原理。缺血后处理如何抑制线粒体通透性转换孔(PTP)的打开以及再灌注时随后心肌细胞的死亡仍然未知。最近的研究表明,沉默调节蛋白3(SIRT3)对亲环蛋白D(CyPD)的脱乙酰作用可以调节其与PIP的结合。

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