Mechanosensitive Piezol Channel Evoked-Mechanical Signals in Atherosclerosis

Recently, more and more works have focused and used extensive resources on atherosclerosis research, which is one of the major causes of death globally. Alongside traditional risk factors, such as hyperlipidemia, smoking, hypertension, obesity, and diabetes, mechanical forces, including shear stress...

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Bibliographic Details
Published inJournal of inflammation research Vol. 14; p. 3621
Main Authors Shinge, Shafiu A. Umar, Zhang, Daifang, Muluh, Tobias Achu, Nie, Yongmei, Yu, Fengxu
Format Journal Article
LanguageEnglish
Published Dove Medical Press Limited 31.07.2021
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Summary:Recently, more and more works have focused and used extensive resources on atherosclerosis research, which is one of the major causes of death globally. Alongside traditional risk factors, such as hyperlipidemia, smoking, hypertension, obesity, and diabetes, mechanical forces, including shear stress, pressure and stretches exerted on endothelial cells by flow, is proved to be crucial in atherosclerosis development. Studies have recognized the mechanosensitive Piezol channel as a special sensor and transducer of various mechanical forces into biochemical signals, and recent studies report its role in atherosclerosis through different mechanical forces in pressure, stretching and turbulent shear stress. Based on our expertise in this field and considering the recent advancement of atherosclerosis research, we will be focusing on the function of Piezol and its involvement in various cellular mechanisms and consequent involvement in the development of atherosclerosis in this review. Also, we will discuss various functions of Piezol involvement in atherosclerosis and come up with new mechanistic insight for future research. Based on the recent findings, we suggest Piezol as a valid candidate for novel therapeutic innovations, in which deep exploration and translating its findings into the clinic will be a new therapeutic strategy for cardiovascular diseases, particularly atherosclerosis. Keywords: atherogenesis, Piezol channel, endothelial cell, inflammation, shear stress, mechanotransduction
ISSN:1178-7031
1178-7031
DOI:10.2147/JIR.S319789