Role of TRPC3 and TRPC6 channels in the myocardial response to stretch: Linking physiology and pathophysiology. (November 2017)

• Record Type: Journal Article
• Authors: Yamaguchi, Yohei; Iribe, Gentaro; Nishida, Motohiro; Naruse, Keiji
• Is Part Of: Progress in biophysics and molecular biology. Volume 130:Part B(2017)
• Page Start: 264
• Page End: 272
• Publication Date: 2017-11
• Subjects: TRPC -- Angiotensin II type 1 receptor -- Ca2+ handling -- Cardiomyocyte -- Cardiac hypertrophy; AT1R angiotensin II type 1 receptor -- BTP 3, 5-bis(trifluoromethyl)pyrazole -- CF carbon fibre -- FSM Frank-Starling mechanism -- NCX Na+/Ca2+ exchanger -- NFAT nuclear factor of activated T cells -- NHE Na+/H+ exchanger -- NOX nicotinamide adenine dinucleotide phosphate oxidase -- NT normal Tyrode solution -- PKG protein kinase G -- PLC phospholipase C -- Pyr3 pyrazole 3 -- ROS reactive oxygen species -- SFR slow force response -- SR sarcoplasmic reticulum -- TRP transient receptor potential -- TRPC transient receptor potential canonical; Biophysics -- Periodicals; Biochemistry -- Periodicals; Biophysics -- Periodicals; Molecular Biology -- Periodicals; Biophysique -- Périodiques; Biochimie -- Périodiques; 571.4
• DOI: 10.1016/j.pbiomolbio.2017.06.010
• Languages: English
• ISSNs: 0079-6107

Abstract

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 Ca 2+ 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 Ca 2+ transient and twitch force during stretch. In the physiological response, a stretch-induced increase in intracellular Ca 2+ 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.