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靶向细胞焦亡的潜在糖尿病性心肌病治疗方法:一篇综述。

Potential diabetic cardiomyopathy therapies targeting pyroptosis: A mini review.

作者信息

Jia Yu, Li Dongze, Yu Jing, Jiang Wenli, Liao Xiaoyang, Zhao Qian

机构信息

General Practice Ward/International Medical Center Ward, General Practice Medical Center, West China Hospital, Sichuan University, Chengdu, China.

Department of Emergency Medicine and National Clinical Research Center for Geriatrics, Disaster Medicine Center, West China Hospital, Sichuan University West China School of Medicine, Chengdu, China.

出版信息

Front Cardiovasc Med. 2022 Aug 18;9:985020. doi: 10.3389/fcvm.2022.985020. eCollection 2022.

Abstract

Pyroptosis is primarily considered a pro-inflammatory class of caspase-1- and gasdermin D (GSDMD)-dependent programmed cell death. Inflammasome activation promotes the maturation and release of interleukin (IL)-1β and IL-18, cleavage of GSDMD, and development of pyroptosis. Recent studies have reported that NLRP3 inflammasome activation-mediated pyroptosis aggravates the formation and development of diabetes cardiomyopathy (DCM). These studies provide theoretical mechanisms for exploring a novel approach to treat DCM-associated cardiac dysfunction. Accordingly, this review aims to summarize studies that investigated possible DCM therapies targeting pyroptosis and elucidate the molecular mechanisms underlying NLRP3 inflammasome-mediated pyroptosis, and its potential association with the pathogenesis of DCM. This review may serve as a basis for the development of potential pharmacological agents as novel and effective treatments for managing and treating DCM.

摘要

细胞焦亡主要被认为是一种依赖半胱天冬酶 -1 和 Gasdermin D(GSDMD)的促炎性程序性细胞死亡。炎性小体激活促进白细胞介素(IL)-1β和 IL-18 的成熟与释放、GSDMD 的切割以及细胞焦亡的发生。最近的研究报道,NLRP3 炎性小体激活介导的细胞焦亡会加重糖尿病性心肌病(DCM)的形成和发展。这些研究为探索治疗 DCM 相关心脏功能障碍的新方法提供了理论机制。因此,本综述旨在总结针对细胞焦亡研究可能的 DCM 治疗方法的研究,并阐明 NLRP3 炎性小体介导的细胞焦亡的分子机制及其与 DCM 发病机制的潜在关联。本综述可为开发潜在的药物制剂作为管理和治疗 DCM 的新型有效疗法提供依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/9433721/60d56c7ecf5c/fcvm-09-985020-g001.jpg

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