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NLRP3 炎性小体在糖尿病心肌病中的作用及其治疗意义。

The Role of NLRP3 Inflammasome in Diabetic Cardiomyopathy and Its Therapeutic Implications.

机构信息

Department of Cardiology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan Province 421001, China.

Cardiovascular Lab of Big Data and Imaging Artificial Intelligence, Hengyang Medical School, University of South China, Hengyang, Hunan Province 421001, China.

出版信息

Oxid Med Cell Longev. 2022 Sep 6;2022:3790721. doi: 10.1155/2022/3790721. eCollection 2022.

Abstract

Diabetic cardiomyopathy (DCM) is a serious complication of diabetes mellitus (DM). However, the precise molecular mechanisms remain largely unclear, and it is still a challenging disease to diagnose and treat. The nucleotide-binding oligomerization domain and leucine-rich repeat pyrin 3 domain (NLRP3) inflammasome is a critical part of the innate immune system in the host to defend against endogenous danger and pathogenic microbial infections. Dysregulated NLRP3 inflammasome activation results in the overproduction of cytokines, primarily IL-1 and IL-18, and eventually, inflammatory cell death-pyroptosis. A series of studies have indicated that NLRP3 inflammasome activation participates in the development of DCM, and that corresponding interventions could mitigate disease progression. Accordingly, this narrative review is aimed at briefly summarizing the cell-specific role of the NLRP3 inflammasome in DCM and provides novel insights into developing DCM therapeutic strategies targeting the NLRP3 inflammasome.

摘要

糖尿病心肌病(DCM)是糖尿病(DM)的严重并发症。然而,确切的分子机制在很大程度上仍不清楚,诊断和治疗仍然是一个具有挑战性的疾病。核苷酸结合寡聚化结构域和富含亮氨酸重复的pyrin 3 结构域(NLRP3)炎性小体是宿主固有免疫系统抵御内源性危险和致病性微生物感染的关键部分。NLRP3 炎性小体的失调激活导致细胞因子(主要是 IL-1 和 IL-18)的过度产生,最终导致炎症细胞死亡-细胞焦亡。一系列研究表明,NLRP3 炎性小体激活参与了 DCM 的发生发展,相应的干预措施可以减轻疾病进展。因此,本综述旨在简要总结 NLRP3 炎性小体在 DCM 中的细胞特异性作用,并为开发针对 NLRP3 炎性小体的 DCM 治疗策略提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cff/9470324/f03a965a847e/OMCL2022-3790721.001.jpg

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