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Pathophysiological Roles of TRPV4 Channel in the Heart
Version 1
: Received: 29 April 2023 / Approved: 30 April 2023 / Online: 30 April 2023 (03:28:24 CEST)
A peer-reviewed article of this Preprint also exists.
Chaigne, S.; Barbeau, S.; Ducret, T.; Guinamard, R.; Benoist, D. Pathophysiological Roles of the TRPV4 Channel in the Heart. Cells 2023, 12, 1654. Chaigne, S.; Barbeau, S.; Ducret, T.; Guinamard, R.; Benoist, D. Pathophysiological Roles of the TRPV4 Channel in the Heart. Cells 2023, 12, 1654.
Abstract
Transient Receptor Potential Vanilloid 4 (TRPV4) channel is a non-selective cation channel, mostly permeable to calcium (Ca2+), which participates to intracellular Ca2+ handling in cardiac cells. It is widely expressed through the body and is activated by a large spectrum of physico-chemical stimuli, conferring it a role in a variety of sensorial and physiological functions. With-in the cardiovascular system, TRPV4 expression was reported in cardiomyocytes, endothelial cells (ECs) and smooth muscle cells (SMCs) where it modulates mitochondrial activity, Ca2+ ho-meostasis, cardiomyocytes electrical activity and contractility, cardiac embryonic development, fibroblast proliferation but also vascular permeability, dilatation and constriction. On the other hand, TRPV4 channels participate in several cardiac pathological processes such as development of cardiac fibrosis, hypertrophy, ischemia-reperfusion injuries, heart failure, myocardial infarc-tion, and arrhythmia. In this manuscript, we provide an overview of TRPV4 channel implica-tions in cardiac physiology and discuss the potential of TRPV4 channel as therapeutic target against cardiovascular diseases.
Keywords
TRPV4 channels; TRPV4-KO mice; heart, myocytes; fibroblasts; action potential, calcium homeo-stasis
Subject
Biology and Life Sciences, Biology and Biotechnology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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