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

Yohei Yamaguchi, Gentaro Iribe, Motohiro Nishida, Keiji Naruse

Research output: Contribution to journalArticle

10 Citations (Scopus)

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.

Original languageEnglish
JournalProgress in Biophysics and Molecular Biology
DOIs
Publication statusAccepted/In press - Jan 30 2017

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Keywords

  • Angiotensin II type 1 receptor
  • Ca handling
  • Cardiac hypertrophy
  • Cardiomyocyte
  • TRPC

ASJC Scopus subject areas

  • Biophysics
  • Molecular Biology

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