Genetic ablation of TRPV1 exacerbates pressure overload-induced cardiac hypertrophy

Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac h...

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Bibliographic Details
Published in:Biomedicine & pharmacotherapy 2018-03, Vol.99, p.261-270
Main Authors: Zhong, Beihua, Rubinstein, Jack, Ma, Shuangtao, Wang, Donna H.
Format: Article
Language:English
Subjects:
Heart
Hypertrophy
Inflammation
Macrophage
TRPV1
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Summary:Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses. Trpv1 knockout (Trpv1−/−) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) or sham operation. Four weeks after TAC, WT and Trpv1-/- mice had developed left ventricular (LV) hypertrophy with increased LV mass, fibrosis and infiltration of macrophages as well as increased secretion of tumor necrosis factor α, interleukin-6 from cardiac tissue (all P 
ISSN:0753-3322
1950-6007
DOI:10.1016/j.biopha.2018.01.065