线粒体功能障碍及线粒体自噬异常在急性胰腺炎中的作用

The role of mitochondrial dysfunction and abnormal mitophagy in acute pancreatitis

急性胰腺炎(AP)是一种尚缺乏特异性治疗方法的胰腺外分泌炎症疾病。目前认为AP的发病主要与胰蛋白酶原异常活化、炎症细胞浸润、钙超载和线粒体功能障碍有关。近年来,越来越多的研究聚焦于AP腺泡细胞的线粒体功能障碍及线粒体自噬功能异常,认为线粒体自噬可以通过降解多余或紊乱的线粒体来维持细胞稳态,改善AP病理损伤。该文综述线粒体功能障碍及其自噬功能异常在AP病理过程中的研究进展,为寻找药物治疗新靶点,减轻AP的临床症状提供新思路。

Acute pancreatitis(AP)is an inflammatory disease of the exocrine pancreas that still lacks specific treatment.At present,the pathogenesis of AP is considered to be mainly related to abnormal activation of trypsinogen,inflammatory cell infiltration,calcium overload,and mitochondrial dysfunction.In recent years,more and more studies have focused on mitochondrial dysfunction and abnormal mitophagy in acinar cells during AP.It is believed that mitophagy maintains cellular homeostasis and attenuates pathological damage in AP by degrading excessive or dysfunctional mitochondria.This review summarizes the research advances in the role of mitochondrial dysfunction and aberrant mitophagy in the pathogenesis of AP,and provides novel insights for establishing new drug targets and alleviating the clinical symptoms of AP.