急性胰腺炎的细胞发病机制研究进展  

Advances in cellular pathogenesis of acute pancreatitis

作　　者：侯文杰 王美堂 HOU Wenjie;WANG Meitang(Department of Emergency,Changhai Hospital of Naval Military Medical University,Shang-hai,200433,China)

机构地区：[1]海军军医大学长海医院急诊科,上海200433

出　　处：《临床急诊杂志》2023年第5期266-271,276,共7页Journal of Clinical Emergency

基　　金：海军军医大学第一附属医院“234学科攀峰计划”项目(No:2020YXK038)

摘　　要：急性胰腺炎(AP)是急诊常见的胰腺炎症性疾病,全球发病率约为34/10万,重症患者预后较差,病死率可达20%~40%。AP的发病机制尚未完全阐明,近年来研究发现,除胰蛋白酶原异常激活外,病理性钙信号、线粒体功能障碍、内质网应激、自噬受损等细胞事件在AP的发生发展中具有重要作用。目前AP的治疗主要是液体复苏、器官支持和并发症处理等,尚无特效治疗药物,了解AP细胞发病机制有助于为其治疗提供新思路,开发新靶点。因此,本文旨在对AP的细胞发病机制作一综述,为其治疗提供新思路。Acute pancreatitis(AP)is a common inflammatory disease of the pancreas in the emergency de-partment with a global incidence of about 34/100,000 and a poor prognosis for severe patients whose mortality rate is 20%to 40%.The pathogenesis of AP has not been fully elucidated.In addition to abnormal activation of trypsinogen,recent studies that cellular events such as pathological calcium signalling,mitochondrial dysfunction,endoplasmic reticulum stress,and impaired autophagy play an important role in the occurrence and development of AP.At present,the treatment of AP is mainly fluid resuscitation,organ support and complication management,there is no effective drug for AP.Understanding the cellular mechanisms of AP may help to provide new ideas for its treatment and identify new targets.Therefore,the purpose of this paper is to review the cellular pathogenesis of AP and provide new ideas for its treatment.

关 键 词：急性胰腺炎 发病机制 胰腺腺泡细胞 研究进展 

分 类 号：R576[医药卫生—消化系统]