Mechanisms of NLRP3 inflammasome in atherosclerosis and advances in targeted inflammatory therapy
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1.Department of Cardiology,Haikou, Hainan 570100, China ;3.Department of Interventional Vascular Surgery,Haikou, Hainan 570100, China ;4.Department of Pharmacy, the First Affiliated Hospital of Hainan Medical University, Haikou, Hainan 570100, China;2.College of Traditional Chinese Medicine, Hainan Medical University, Haikou, Hainan 570100, China)

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R5

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    Abstract:

    Atherosclerosis (As) is a pathological process caused by a complex set of factors, including endothelial dysfunction, lipid deposition in the arterial vessel wall, macrophage infiltration, smooth muscle cell dysfunction, and foam cell formation, in which inflammatory response plays an indispensable role. NOD-like receptor protein 3(NLRP3) inflammasomes are transducers of inflammatory cells, and NLRP3 inflammasome activation mediates the inflammatory response and activates downstream interleukin-18 and interleukin-1β, thereby participating in the occurrence and development of As. Therefore, specific inhibitors targeting NLRP3 inflammasome and downstream inflammatory factors are potential targets for current clinical drug research and are expected to be a new therapeutic measure for treating As. In this article, the mechanism of NLRP3 inflammasome and the relationship with As are discussed, and drugs targeting NLRP3 inflammasome and downstream inflammatory factors are also described.

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MENG Qingwen, LIU Huajiang, YI Hongru, LIU Qibing. Mechanisms of NLRP3 inflammasome in atherosclerosis and advances in targeted inflammatory therapy[J]. Editorial Office of Chinese Journal of Arteriosclerosis,2024,32(1):79-86.

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History
  • Received:June 26,2023
  • Revised:August 14,2023
  • Online: February 05,2024
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