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NLRP3炎性小体:心血管疾病领域的后起之秀。

NLRP3 inflammasome: The rising star in cardiovascular diseases.

作者信息

Zheng Yidan, Xu Li, Dong Nianguo, Li Fei

机构信息

Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

出版信息

Front Cardiovasc Med. 2022 Sep 20;9:927061. doi: 10.3389/fcvm.2022.927061. eCollection 2022.

Abstract

Cardiovascular diseases (CVDs) are the prevalent cause of mortality around the world. Activation of inflammasome contributes to the pathological progression of cardiovascular diseases, including atherosclerosis, abdominal aortic aneurysm, myocardial infarction, dilated cardiomyopathy, diabetic cardiomyopathy, heart failure, and calcific aortic valve disease. The nucleotide oligomerization domain-, leucine-rich repeat-, and pyrin domain-containing protein 3 (NLRP3) inflammasome plays a critical role in the innate immune response, requiring priming and activation signals to provoke the inflammation. Evidence shows that NLRP3 inflammasome not only boosts the cleavage and release of IL-1 family cytokines, but also leads to a distinct cell programmed death: pyroptosis. The significance of NLRP3 inflammasome in the CVDs-related inflammation has been extensively explored. In this review, we summarized current understandings of the function of NLRP3 inflammasome in CVDs and discussed possible therapeutic options targeting the NLRP3 inflammasome.

摘要

心血管疾病(CVDs)是全球普遍的死亡原因。炎性小体的激活促成了心血管疾病的病理进展,包括动脉粥样硬化、腹主动脉瘤、心肌梗死、扩张型心肌病、糖尿病心肌病、心力衰竭和钙化性主动脉瓣疾病。含核苷酸寡聚化结构域、富含亮氨酸重复序列和吡啉结构域的蛋白3(NLRP3)炎性小体在固有免疫反应中起关键作用,需要启动和激活信号来引发炎症。有证据表明,NLRP3炎性小体不仅促进IL-1家族细胞因子的切割和释放,还会导致一种独特的细胞程序性死亡:焦亡。NLRP3炎性小体在与CVDs相关的炎症中的重要性已得到广泛探索。在本综述中,我们总结了目前对NLRP3炎性小体在CVDs中的功能的认识,并讨论了针对NLRP3炎性小体的可能治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f4a/9530053/b22d38e0580f/fcvm-09-927061-g0001.jpg

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