细胞焦亡在脓毒症心肌抑制中的作用研究进展  

Recent research on pyroptosis in sepsis-induced myocardial depression

作　　者：文日 张铁凝(综述) 杨妮[1] 刘春峰(审校)[1] WEN Ri;ZHANG Tie-Ning;YANG Ni;LIU Chun-Feng(Department of Pediatric Intensive Care Unit,Shengjing Hospital,China Medical University,Shenyang 110004,China)

机构地区：[1]中国医科大学附属盛京医院儿童急诊与重症医学科,辽宁沈阳110004

出　　处：《中国当代儿科杂志》2024年第7期774-781,共8页Chinese Journal of Contemporary Pediatrics

基　　金：国家自然科学基金项目(81971810;82002021)。

摘　　要：脓毒症心肌抑制是脓毒症患者常见的并发症,是脓毒症患者死亡的主要原因之一。其发病机制复杂,目前尚无统一定论。细胞焦亡是一种促炎的程序性细胞死亡,其特点是Gasdermins家族介导的细胞膜孔洞形成、细胞肿胀、细胞破裂,伴随大量炎症因子等细胞内容物的释放。细胞焦亡在多种炎症相关疾病中扮演了重要角色,主要通过胱天蛋白酶(caspase)-1介导的经典通路和caspase-4/5/11介导的非经典通路发挥作用。越来越多的研究表明细胞焦亡参与脓毒症心肌抑制的发生发展。该文围绕细胞焦亡的分子学机制及其在脓毒症心肌抑制中的研究进展进行综述,以期为脓毒症心肌抑制的治疗提供新策略与新靶点。Sepsis-induced myocardial depression(SIMD),a common complication of sepsis,is one of the main causes of death in patients with sepsis.The pathogenesis of SIMD is complicated,and the process of SIMD remains incompletely understood,with no single or definitive mechanism fully elucidated.Notably,pyroptosis,as a proinflammatory programmed cell death,is characterized by Gasdermin-mediated formation of pores on the cell membrane,cell swelling,and cell rupture accompanied by the release of large amounts of inflammatory factors and other cellular contents.Mechanistically,pyroptosis is mainly divided into the canonical pathway mediated by caspase-1 and the noncanonical pathway mediated by caspase-4/5/11.Pyroptosis has been confirmed to participate in various inflammationassociated diseases.In recent years,more and more studies have shown that pyroptosis is also involved in the occurrence and development of SIMD.This article reviews the molecular mechanisms of pyroptosis and its research progress in SIMD,aiming to provide novel strategies and targets for the treatment of SIMD.

关 键 词：脓毒症 心肌抑制 细胞焦亡 

分 类 号：R459.7[医药卫生—急诊医学]