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炎症小体作为动脉粥样硬化的治疗靶点:聚焦钾外流

Inflammasome as a Therapeutic Target for Atherosclerosis: A Focus on Potassium Outflow.

作者信息

Jin Yi-Jing, An Zhuo-Yu, Sun Zhi-Xuan, Liu Xin-Chen

机构信息

Peking University Health Science Center, 100191 Beijing, China.

Department of Cardiology, Peking University First Hospital, 100034 Beijing, China.

出版信息

Rev Cardiovasc Med. 2022 Jul 22;23(8):268. doi: 10.31083/j.rcm2308268. eCollection 2022 Aug.

DOI:10.31083/j.rcm2308268
PMID:39076616
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11266955/
Abstract

Atherosclerosis is a risk factor for various cardiovascular diseases, and is linked to high rates of morbidity and mortality across the globe. Although numerous complex processes are involved in the development and progression of atherosclerosis, the exact mechanisms behind its pathogenesis remain unclear. Inflammation and endothelial cell damage exert a lasting effect on atherosclerosis, causing lipid and fibrous tissue accumulation in the intima of the artery to form plaques, and subsequently promoting atherosclerosis. Nod-like receptor protein 3 () inflammatory corpuscle is thought to be the link between lipid metabolism and inflammation. Long Potassium outflow is a vital activator of , with a simultaneous effect as a start-up and adjustment. The majority of existing drugs for atherosclerosis targeting the signaling pathway target IL-1, whereas drugs targeting the critical link of potassium efflux are relatively new. This review discusses the inflammatory corpuscle as a critical regulator of the immunological inflammatory pathway in atherosclerosis. Moreover, current knowledge on inflammatory corpuscle start and activation pathways were integrated, emphasizing potassium-involved outflow-related proteins. We highlight potential treatment approaches for inflammatory corpuscle pathways, specifically targeting potassium outflow channels of targeted drugs. Collectively, these insights indicate that targeting the inflammatory corpuscle is a vital anti-inflammatory therapy for treating atherosclerosis.

摘要

动脉粥样硬化是多种心血管疾病的危险因素,与全球范围内的高发病率和死亡率相关。尽管动脉粥样硬化的发生和发展涉及众多复杂过程,但其发病机制背后的确切机制仍不清楚。炎症和内皮细胞损伤对动脉粥样硬化产生持久影响,导致脂质和纤维组织在动脉内膜积聚形成斑块,进而促进动脉粥样硬化。Nod样受体蛋白3()炎性小体被认为是脂质代谢与炎症之间的联系。长时程钾外流是炎性小体的重要激活剂,同时具有启动和调节作用。现有的大多数针对动脉粥样硬化的药物靶向炎性小体信号通路中的白细胞介素-1,而针对钾外流关键环节的药物相对较新。本综述讨论了炎性小体作为动脉粥样硬化中免疫炎症途径的关键调节因子。此外,整合了关于炎性小体启动和激活途径的现有知识,强调了与钾外流相关的蛋白质。我们重点介绍了针对炎性小体途径的潜在治疗方法,特别是靶向药物的钾外流通道。总体而言,这些见解表明,靶向炎性小体是治疗动脉粥样硬化的重要抗炎疗法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa47/11266955/b1e045e822fe/2153-8174-23-8-268-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa47/11266955/e981cac0e352/2153-8174-23-8-268-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa47/11266955/b1e045e822fe/2153-8174-23-8-268-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa47/11266955/e981cac0e352/2153-8174-23-8-268-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa47/11266955/b1e045e822fe/2153-8174-23-8-268-g2.jpg

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