急性胰腺炎的发病机制研究进展及未来展望  

Research progress and future prospect on the pathogenesis of acute pancreatitis

作　　者：彭凯新 文礼 PENG Kaixin;WEN Li(Biomarker Discovery and Validation Platform,Peking Union Medical College Hospital,Chinese Academy of Medical Sciences,Beijing 100005,China)

机构地区：[1]北京协和医院/中国医学科学院临床医学研究所,生物标志物研究平台,北京100005

出　　处：《西安交通大学学报（医学版）》2024年第2期167-177,共11页Journal of Xi’an Jiaotong University（Medical Sciences）

基　　金：国家自然科学基金资助项目(No.82122010,No.82070659);中央高水平医院临床科研专项(No.2022-PUMCH-E-003);中国医学科学院医学与健康科技创新工程项目(No.2023-I2M-3-001)。

摘　　要：急性胰腺炎(acute pancreatitis,AP)是消化系统常见急腹症之一,发病率在我国和欧美各国均呈逐年上升趋势。尽管病因多种多样,但均遵循特定的病理生理学过程且其中的关键调控分子具有相似性。近年来,一方面以胰腺腺泡和导管上皮细胞为主要研究对象,聚焦钙信号通路、自噬流受损、线粒体等细胞器功能障碍、内质网应激失衡取得了不少重要进展;另一方面聚焦免疫细胞的早期募集和过度活化参与调控全身炎症反应的发生及胰腺坏死和胰腺炎相关器官功能不全开展了不少前沿研究。上述研究发现大大增进了我们对AP发病机制和干预策略的理解和认识。本文将重点讨论近年来AP发病机制的基础研究进展,以期对AP的早期治疗提供临床指导。Acute pancreatitis(AP) is one of the common acute abdominal diseases of the digestive system,and its incidence is increasing year by year in China,Europe,and the United States.Although its etiology is diverse,it follows certain pathophysiological processes and the key regulatory molecules are similar.Over the past few years,on the one hand,progress in the research was made on pancreatic acinar and ductal epithelial cells including calcium signaling pathways,impaired autophagy flux,dysfunction of mitochondria and other organelles,and endoplasmic reticulum stress imbalance.On the other hand,important progress was made in early recruitment and excessive activation of immune cells and their roles in regulating pancreatic necrosis and pancreatitis-associated multiple organ failure.All of the above-mentioned research progress has greatly enhanced our understanding of the pathogenesis and intervention strategies of AP.This article will focus on the basic research progress in the pathogenesis of AP in recent years in order to provide clinical guidance for the early treatment of AP.

关 键 词：急性胰腺炎 发病机制 钙信号 自噬 细胞器 免疫细胞 脂毒性 

分 类 号：R576[医药卫生—消化系统]