4.7 Review

Emerging Piezo1 signaling in inflammation and atherosclerosis; a potential therapeutic target

期刊

出版社

IVYSPRING INT PUBL
DOI: 10.7150/ijbs.63819

关键词

Atherosclerosis; Piezo1 channel; Endothelial cell; Inflammation; shear stress; mechanomedicine

资金

  1. National Natural Science Foundation of China [31860261, 11462022]
  2. Collaborative Innovation Center for Prevention and Treatment of Cardiovascular Disease of Sichuan Province [xtcx2019-03, xtcx2019-04]
  3. Luzhou Municipal People's Government - Southwest Medical University Science and Technology Strategic Cooperation Project [2018LZXNYD-ZK27, 2018LZXNYD-ZK40]

向作者/读者索取更多资源

This review highlights the role of mechanosensitive protein Piezo1 in atherosclerosis and its therapeutic potentials. Recent studies have shown that Piezo1 channel acts as a sensor and transducer of mechanical forces, affecting various cellular activities involved in atherosclerosis, such as proliferation, migration, apoptosis, and vascular remodeling. Understanding the mechanisms of Piezo1 and its drugability may lead to novel therapeutic strategies for treating atherosclerosis and other cardiovascular diseases.
Purpose of Review: Atherosclerosis is the principal cause of cardiovascular diseases (CVDs) which are the major cause of death worldwide. Mechanical force plays an essential role in cardiovascular health and disease. To bring the awareness of mechanosensitive Piezo1 role in atherosclerosis and its therapeutic potentials we review recent literature to highlight its involvement in various mechanisms of the disease. Recent Findings: Recent studies reported Piezo1 channel as a sensor, and transducer of various mechanical forces into biochemical signals, which affect various cellular activities such as proliferation, migration, apoptosis and vascular remodeling including immune/inflammatory mechanisms fundamental phenomenon in atherogenesis. Summary: Numerous evidences suggest Piezo1 as a player in different mechanisms of cell biology, including immune/inflammatory and other cellular mechanisms correlated with atherosclerosis. This review discusses mechanistic insight about this matter and highlights the drugability and therapeutic potentials consistent with emerging functions Piezo1 in various mechanisms of atherosclerosis. Based on the recent works, we suggest Piezo1 as potential therapeutic target and a valid candidate for future research. Therefore, a deeper exploration of Piezo1 biology and translation towards the clinic will be a novel strategy for treating atherosclerosis and other CVDs.

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