Dietary capsaicin ameliorates pressure overload-induced cardiac hypertrophy and fibrosis through the transient receptor potential vanilloid type 1.

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Dietary capsaicin plays a protective role in hypertension, atherosclerosis, obesity, and hyperlipidemia through activating the transient receptor potential vanilloid type 1 (TRPV1), a nonselective cation channel. This study was designed to investigate the role of capsaicin in cardiac hypertrophy and fibrosis in a pressure overload model. TRPV1 knockout (KO) mice and their wild-type (WT) littermates, aged 8 weeks, were randomly divided into sham and aortic banding surgery groups and were fed with chow or chow plus capsaicin for 10 weeks. Dietary capsaicin significantly attenuates pressure overload-induced increase in heart weight index, enlargement of ventricular volume, decrease in cardiac function, and increase in cardiac fibrosis in WT mice. However, these effects of capsaicin were absent in TRPV1 KO mice. Additionally, capsaicin blunted pressure overload-induced upregulation of transforming growth factor β, connective tissue growth factor, and the phosphorylation of Smad2/3 in WT mice but not in TRPV1 KO mice. Moreover, capsaicin attenuated pressure overload-induced overexpression of metalloproteinase (MMP)-2, MMP-9 and MMP-13 in WT mice but not in TRPV1 KO mice. Capsaicin also attenuated angiotensin II-induced proliferation of cardiac fibroblasts from mice with the TRPV1 channel. Our results suggest that dietary capsaicin protects against cardiac hypertrophy and fibrosis in pressure overload mice through TRPV1.