细胞焦亡在草酸钙肾结石形成机制中的研究进展  

Research progress of pyroptosis in calcium oxalate renal calculi formation

作　　者：向近杰(综述) 李颢(审校)[1] XIANG Jinjie;LI Hao(Department of Urology,The First Affiliated Hospital of Kunming Medical University,Kunming 650032,China)

机构地区：[1]昆明医科大学第一附属医院泌尿外科,昆明650032

出　　处：《肾脏病与透析肾移植杂志》2023年第2期168-173,共6页Chinese Journal of Nephrology,Dialysis & Transplantation

基　　金：云南省科技厅科技计划项目(202001AY070001-158)。

摘　　要：细胞焦亡是由半胱天冬酶(caspase)家族介导的一种新的程序性细胞死亡,其机制是caspase-1通过不同的炎症小体激活,裂解底物gasdermin D(GSDMD)后在细胞膜上形成孔隙并释放促炎症因子导致免疫炎症反应的发生。研究表明,细胞焦亡在草酸钙诱导肾结石的形成过程中发挥着重要作用,主要与肾小管上皮细胞发生氧化应激损伤和草酸钙晶体黏附性增加有关。本文就细胞焦亡相关分子机制以及在肾小管上皮细胞损伤和草酸钙结石形成中的研究进展作一综述,为未来肾结石的发病机制研究提供参考。Pyroptosis is a new type of programmed cell death mediated by the caspase family.The mechanism is that caspase-1 is activated by different inflammasomes,and forms pores in cell membrane after cleavage of substrate gasdermin D(GSDMD),and releases pro-inflammatory factors,leading to immune inflammatory response.Recent studies have shown that pyroptosis plays an important role in the formation of renal calculi induced by calcium oxalate,which is mainly manifested by oxidative stress damage of renal tubular epithelial cells and increase of calcium oxalate crystal adhesion.This review provided an overview of the molecular mechanism of pyroptosis and research progress in renal tubular epithelial cell injury and calcium oxalate stone formation,providing reference for pathogenesis of kidney stones in the future.

关 键 词：细胞焦亡 炎症小体 肾小管上皮细胞 草酸钙结石 

分 类 号：R692.4[医药卫生—泌尿科学]