自噬在急性胰腺炎中的研究新进展

New research progress of autophagy in acute pancreatitis

自噬是细胞清除胞质中受损、缺陷或无用的细胞器、长寿命蛋白质和脂质,并回收其成分以满足生物新陈代谢的营养和能量需要的主要分解代谢过程。急性胰腺炎(AP)是常见临床急症,其发病率也逐年升高。研究显示,自噬在AP的发病过程中起到重要作用,可以导致胰腺腺泡细胞内胰蛋白酶原的激活,腺泡细胞内大液泡积聚,诱发促炎介质的释放,引起胰腺炎症细胞浸润和全身性炎症反应。笔者就自噬的分子机制以及自噬在AP发生、发展中作用机制的研究进展进行综述。

Autophagy is a major catabolic process in which cells remove damaged,defective or useless organelles,long-lived proteins and lipids from the cytoplasm,and recycle their components to meet the nutritional and energy needs of biological metabolism.Acute pancreatitis(AP)is a common critical disease,and its prevalence continues to rise in recent years.Studies have demonstrated that autophagy plays an important role in the pathogenesis of AP,it can cause trypsinogen activation and accumulation of large vacuoles in the pancreatic acinar cells,and induce the release of proinflammatory mediators,and thereby cause inflammatory cell infiltration of the pancreas and systemic inflammatory response.Here,the authors address the molecular mechanism of autophagy and the mechanism of autophagy in the occurrence and development of AP.