自噬在急性胰腺炎中的研究进展

Advances in the role of autophagy in acute pancreatitis

自噬是细胞通过清除细胞内的有害蛋白或陈旧结构,进行自我保护的细胞机制.急性胰腺炎（AP）的发生与自噬有密切关系,主要表现为异常自噬直接启动AP或AP发生后异常自噬加重AP病情.本文通过相关文献综述,阐明在AP中,自噬异常的主要原因为组织蛋白酶和溶酶体膜相关蛋白功能异常,表现为胰腺腺泡细胞空泡积累,自噬溶酶体形成障碍,最终导致胰酶的提前激活.异常自噬主要通过高迁移率族蛋白B1（HMGB1）再分布和促进线粒体通透性转换两种机制加重AP病情.了解上述机制,对AP的防治具有一定意义.

Autophagy is a self-protect cellular mechanism by which the unneeded cellular structure or impaired protein are targeted to degeneration. Acute pancreatitis （AP） is associated with autophagy tightly. This article is aimed to mainly elaborate the phenomenon that AP can be triggered by impaired autophagy and the mechanism of AP exacerbation by damaged autophagy. In AP, the reasons of impaired autophagy is dysfunction of cathepsins and lysosome associated membrane protein, which present as vacuoles accumulation in acinar cells and combination disorder of autophagolysosome, finally to activation of trypsin. By the relocation of high mobility group box 1 （HMGB1） and promotion of mitochondrial permeability transition （MPT）, impaired autophagy aggravates AP. Understanding the above mechanism has certain significance to the prevention and treatment of AP.