缺血再灌注损伤下微囊泡抑制心肌细胞凋亡的研究进展

Mechanisms of microvesicles inhibiting cardiomyocyte apoptosis under ischemia-reperfusion injury

细胞凋亡是心肌细胞缺血后再灌注导致心肌细胞损伤的主要形式之一,近年来的研究发现,微囊泡可由缺血再灌注损伤后的细胞释放,并参与包括细胞凋亡在内的多种不同的病理生理过程。在此,我们概括了缺血再灌注过程中心肌细胞所释放的微囊泡的特征,并总结了微囊泡抑制心肌细胞凋亡的可能分子机制,最后我们初步概括微囊泡在缺血再灌注相关心脏疾病中的作用,这可能为今后心脏缺血性疾病的治疗提供新思路。

Apoptosis as a means of cell death,is one of the major mechanisms of cardiomyocytes death immediately following a short period of ischemia with ensuing reperfusion.In recent years,accumulating studies have observed that microvesicles(MVs)could be released from ischemia-reperfusion(I/R)injured cells and mediate both physiological and pathological processes,including apoptosis.Herein,we summarized the characteristics of MVs released from cardiomyocytes during the process of I/R.Furthermore,we concluded the molecular mechanisms of anti-apoptosis mediated by I/R cell-derived MVs.At last,we emphasized the vital benefits and potential treatments of MVs in I/R-related diseases,which may provide new ideas for the treatment of ischemic heart diseases in the future.