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

Yohei Yamaguchi, Gentaro Iribe, Motohiro Nishida, Keiji Naruse

研究成果: Contribution to journalReview article査読

20 被引用数 (Scopus)

抄録

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.

本文言語英語
ページ(範囲)264-272
ページ数9
ジャーナルProgress in Biophysics and Molecular Biology
130
DOI
出版ステータス出版済み - 11 2017
外部発表はい

All Science Journal Classification (ASJC) codes

  • 生物理学
  • 分子生物学

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