Research Project
Grant-in-Aid for Scientific Research (C)
Dilated cardiomyopathy (DCM) is a severe disorder defined by ventricular dilation and cardiac dysfunction. A subset of familial DCM is caused by mutations of the genes encoding cytoskeleton. Here, we show that transient receptor potential vanilloid 2 (TRPV2) is highly concentrated in the ventricular sarcolemma of patients with idiopathic DCM and animal models of cardiomyopathy. We found some tools to inhibit the surface expression of and Ca2+ influx via TRPV2. In the animal models, blockade of TRPV2 ameliorated cardiac dysfunction, and prevented DCM progression; Therefore, we propose that sarcolemmal accumulation or activation of TRPV2 initiated by membrane instability resulting from cytoskeleton abnormalities contributes to cardiac dysfunction in DCM, and TRPV2 may be a promising therapeutic target for advanced heart failure.
All 2014 2013 2012 2011 Other
All Journal Article (4 results) (of which Peer Reviewed: 4 results) Presentation (29 results) (of which Invited: 1 results) Book (5 results) Remarks (4 results) Patent(Industrial Property Rights) (1 results) (of which Overseas: 1 results)
Cardiovascular Research
Volume: 99 Issue: 4 Pages: 760-768
10.1093/cvr/cvt163
J Mol Cell Cardiol
Volume: 59 Pages: 76-85
10.1016/j.yjmcc.2013.02.008
Muscle & Nerve
Volume: 47(3) Issue: 3 Pages: 372-378
10.1002/mus.23632
Cardiovasc Res
Volume: 99 Pages: 760-768
http://www.ncvc.go.jp/res/bunshi/bunshij.html
http://www.ncvc.go.jp/res/divisions/molecular_physiology/mp_002.html
