Abstract

Transient receptor potential vanilloid type 1 (TRPV1) is a non-selective cation channel, which is involved in the endogenous stress adaptation mechanism for protection of the heart as well as the occurrence and development of some heart diseases. Although the effect of activation of the TRPV1 channel on different types of non-neural cells in the heart remains unclear, most data show that stimulation of sensory nerves expressing TRPV1 or stimulation/overexpression of the TRPV1 channel has a beneficial role in heart disease. Some studies have proven that TRPV1 has an important relationship with pathological myocardial hypertrophy, but the specific mechanism and effect are not clear. In order to help researchers better understand the relationship between TRPV1 and pathological myocardial hypertrophy, this paper aims to summarize the effect of TRPV1 and the related mechanism in the occurrence and development of pathological myocardial hypertrophy from the following three points of view: 1) role of TRPV1 in alleviation of pathological myocardial hypertrophy; 2) role of TRPV1 in aggravation of pathological myocardial hypertrophy; and 3) the point of view of our team of researchers. It is expected that new therapies can provide potential targets for pathological myocardial hypertrophy.

Highlights

  • Transient Receptor Potential Vanilloid Type 1Transient receptor potential cation channel, subfamily V, member 1 (TRPV1), is a widely reported non-selective cation channel

  • This study suggests that the mitogen-activated protein kinase (MAPK) signalling pathway and intracellular polyamines are important in TRPV1-induced cardiac hypertrophy (Chen et al, 2016)

  • Myocardial hypertrophy increases the work of myocardial cells through the thickening of the ventricular wall, so as to maintain the heart pumping blood to meet the needs of peripheral organs under the condition of increased load

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Summary

Introduction

Transient Receptor Potential Vanilloid Type 1Transient receptor potential cation channel, subfamily V, member 1 (TRPV1), is a widely reported non-selective cation channel. TRPV1 can be activated or inhibited by a variety of physical or chemical substances. Its agonists, such as capsaicin, are the most commonly used as analgesic agents. After TRPV1 activation, nerve permeability to calcium ions increases and intracellular calcium ion levels rise, leading to nerve stimulation. This stimulation can be conducted upward to the central nervous system to form an autonomic reflex and can prompt the sensory nerve terminals locally to release neurotransmitters, including somatostatin (SOM), calcitonin gene-related peptide (CGRP), substance P(SP), and other neuropeptides (Levite et al, 1998; Okajima and Harada, 2006)

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