Physiological and Pathological Role of TRPV1, TRPV2 and TRPV4 Channels in Heart

Overview

Journal Curr Cardiol Rev

Publisher Bentham Science Publishers

Specialty Cardiology & Vascular Diseases

Date 2019 Mar 9

PMID 30848206

Citations 11

Authors

Alexandr S Gorbunov

Leonid N Maslov

Amteshwar S Jaggi

Nirmal Singh

Luciano De Petrocellis

Alla A Boshchenko

Ali Roohbakhsh

Vladimir V Bezuglov

Peter R Oeltgen

Affiliations

Soon will be listed here.

Abstract

Transient receptor potential vanilloid channel 2 (TRPV2) is required for normal cardiac contractility. The stimulation of TRPV1 in isolated cardiomyocytes can aggravate the effect of hypoxia/ reoxygenation (H/R) on H9C2 cells. The knockout of the TRPV1 gene promotes increased tolerance of the isolated perfused heart to the impact of ischemia/reperfusion (I/R). However, activation of TRPV1 increases the resistance of the heart to I/R due to calcitonin gene-related peptide (CGRP) release from afferent nerve endings. It has been established that TRPV1 and TRPV2 are involved in the pathogenesis of myocardial infarction and, in all likelihood, ensure the cardiac tolerance to the ischemia/reperfusion. It has also been documented that the activation of TRPV4 negatively affects the stability of cardiomyocytes to the H/R. The blockade of TRPV4 can be considered as a new approach to the prevention of I/R injury of the heart. Studies also indicate that TRPV1 is involved in the pathogenesis of cardiac hypertrophy and that TRPV2 channels participate in the pathogenesis of dilated cardiomyopathy. Excessive expression of TRPV2 leads to chronic Ca2+- overload of cardiomyocytes, which may contribute to the development of cardiomyopathy.

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