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Review
. 2017 Nov;130(Pt B):264-272.
doi: 10.1016/j.pbiomolbio.2017.06.010. Epub 2017 Jun 20.

Role of TRPC3 and TRPC6 channels in the myocardial response to stretch: Linking physiology and pathophysiology

Yohei Yamaguchi  1 , Gentaro Iribe  2 , Motohiro Nishida  3 , Keiji Naruse  4
Affiliations
Review

Role of TRPC3 and TRPC6 channels in the myocardial response to stretch: Linking physiology and pathophysiology

Yohei Yamaguchi et al. Prog Biophys Mol Biol. 2017 Nov.

Abstract

Transient receptor potential (TRP) channels constitute a large family of versatile multi-signal transducers. In particular, TRP canonical (TRPC) channels are known as receptor-operated, non-selective cation channels. TRPC3 and TRPC6, two members in the TRPC family, are highly expressed in the heart, and participate in the pathogenesis of cardiac hypertrophy and heart failure as a pathological response to chronic mechanical stress. In the pathological response, myocardial stretch increases intracellular Ca2+ levels and activates nuclear factor of activated T cells to induce cardiac hypertrophy. Recent studies have revealed that TRPC3 and TRPC6 also contribute to the physiological stretch-induced slow force response (SFR), a slow increase in the Ca2+ transient and twitch force during stretch. In the physiological response, a stretch-induced increase in intracellular Ca2+ mediated by TRPC3 and TRPC6 causes the SFR. We here overview experimental evidence of the involvement of TRPC3 and TRPC6 in cardiac physiology and pathophysiology in response to stretch.

Keywords: Angiotensin II type 1 receptor; Ca(2+) handling; Cardiac hypertrophy; Cardiomyocyte; TRPC.

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