急性胰腺炎发病机制的研究进展

Research advances on the pathogenesis of acute pancreatitis

急性胰腺炎(AP)是胰腺的炎症性疾病,其发病机制除与胰蛋白酶原异常激活相关外,还与钙超载、线粒体功能障碍、自噬受损和内质网应激相关,发病机制尚未完全阐明。目前尚无有效治疗AP的方案,难以防止胰腺功能的丧失。深入了解AP的病理生理机制有助于找到潜在的治疗靶点。因而,本文旨在对AP发病机制做一综述,为治疗提供更多的研究方向。

Acute pancreatitis(AP)is an inflammatory disease of the pancreas.Its pathogenesis is not only related to abnormal activation of trypsinogen,but also related to calcium overload,mitochondrial dysfunction,impaired autophagy and endoplasmic reticulum stress.However,the mechanism has not been fully elucidated and needs to be further studied.Currently,there is no effective treatment for AP.It is difficult to prevent the loss of pancreatic function.An in-depth understanding of the pathophysiological mechanisms of AP may help to identify the potential therapeutic targets.Therefore,the purpose of this study is to review recent advances in the mechanism of AP in order to provide more research direction for treatment.