Wen Ri, Zhang Tie-Ning, Yang Ni
Department of Pediatric Intensive Care Unit, Shengjing Hospital, China Medical University, Shenyang 110004, China.
Zhongguo Dang Dai Er Ke Za Zhi. 2024 Jul 15;26(7):774-781. doi: 10.7499/j.issn.1008-8830.2312039.
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 pro-inflammatory 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 non-canonical pathway mediated by caspase-4/5/11. Pyroptosis has been confirmed to participate in various inflammation-associated 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.
脓毒症诱导的心肌抑制(SIMD)是脓毒症的常见并发症,是脓毒症患者死亡的主要原因之一。SIMD的发病机制复杂,其过程仍未完全阐明,尚无单一或明确的机制得到充分阐释。值得注意的是,细胞焦亡作为一种促炎性程序性细胞死亡,其特征在于Gasdermin介导的细胞膜上形成孔道、细胞肿胀以及细胞破裂,并伴有大量炎性因子和其他细胞内容物的释放。从机制上讲,细胞焦亡主要分为由caspase-1介导的经典途径和由caspase-4/5/11介导的非经典途径。细胞焦亡已被证实参与各种炎症相关疾病。近年来,越来越多的研究表明,细胞焦亡也参与SIMD的发生和发展。本文综述了细胞焦亡的分子机制及其在SIMD中的研究进展,旨在为SIMD的治疗提供新的策略和靶点。