急性胰腺炎中程序性细胞死亡的研究进展  

Research Progress on Programmed Cell Death in Acute Pancreatitis

作　　者：何天阳 信立霞 张佃良 

机构地区：[1]大连医科大学研究生院,辽宁 大连 [2]滨州医学院烟台附属医院肾内科,山东 烟台 [3]青岛市市立医院胃肠外科,山东 青岛

出　　处：《临床医学进展》2024年第5期503-511,共9页Advances in Clinical Medicine

摘　　要：急性胰腺炎(acute pancreatitis, AP)作为一种自限性腹部疾病,未能及时有效地治疗或将发展成为重症急性胰腺炎(severe acute pancreatitis, SAP),往往导致毁灭性的炎症反应及器官障碍。在此过程中,涉及紧密的信号通路和分子效应机制,精准地调控程序性细胞死亡(programmed cell death, PCD),包括凋亡、自噬、程序性坏死、焦亡、铁死亡及铜死亡。针对PCD的探究,了解其内在相互交错的级联通路,有助于进一步探寻AP的发病机制,为临床治疗找寻新的方向。Acute pancreatitis (AP) as a self-limiting abdominal disease, if not treated promptly and effectively, can develop into severe acute pancreatitis (SAP), often leading to destructive inflammatory reactions and organ dysfunction. In this process, closely linked signaling pathways and molecular effect mechanisms precisely regulate programmed cell death (PCD), including apoptosis, autophagy, programmed necrosis, necroptosis, ferroptosis, and cuproptosis. Exploring PCD and understanding its intrinsic interwoven cascade pathways can help further explore the pathogenesis of AP and seek new directions for clinical treatment.

关 键 词：急性胰腺炎 程序性细胞死亡 铁死亡 

分 类 号：R57[医药卫生—消化系统]