自噬在肝缺血再灌注损伤中的研究进展

Role of autophagy in hepatic ischemia-reperfusion injury

肝缺血再灌注损伤(ischemia reperfusion injury,IRI)是包括肝叶切除术和肝移植术在内的外科手术过程中引起肝脏损伤的重要原因,也是导致移植术后肝功能衰竭的主要潜在因素.肝IRI的发生机制复杂而多样,涉及众多环节.自噬是一个进化上高度保守的过程,可降解受损和功能障碍的细胞成分如线粒体与脂质等,调节肝IRI时细胞的稳态和存活能力.本文系统性介绍肝IRI的分子机制、自噬的功能以及以自噬作为靶点治疗肝IRI的前景.

Hepatic ischemia-reperfusion injury（IRI） is a crucial cause of liver damage occurring in some surgical procedures including hepatic resection and liver transplantation, and it remains the key potential cause of hepatic failure after liver transplantation. The mechanism of hepatic IRI is diverse and complicated, and involves various stages. Autophagy, an evolutionarily conserved process responsible for the degradation of damaged and dysfunctional cytoplasmic contents such as mitochondrion and lipids, regulates cellular homeostasis and survival during hepatic IRI. This review summarizes the molecular mechanisms underlying hepatic IRI, epitomizes the functions of autophagy, and describes the prospects of using autophagy as a therapeutic target for hepatic IRI.