Combined TRPC3 and TRPC6 blockade by selective small-molecule or genetic deletion inhibits pathological cardiac hypertrophy-Reference-Cited by-同舟云学术

Combined TRPC3 and TRPC6 blockade by selective small-molecule or genetic deletion inhibits pathological cardiac hypertrophy

Published:2014-01-22 Issue:4 Volume:111 Page:1551-1556
ISSN:0027-8424
Container-title:Proceedings of the National Academy of Sciences
language:en
Short-container-title:Proceedings of the National Academy of Sciences

Author:

Seo K.,Rainer P. P.,Shalkey Hahn V.,Lee D.-i.,Jo S.-H.,Andersen A.,Liu T.,Xu X.,Willette R. N.,Lepore J. J.,Marino J. P.,Birnbaumer L.,Schnackenberg C. G.,Kass D. A.

Publisher

Proceedings of the National Academy of Sciences

Subject

Multidisciplinary

Reference37 articles.

1. Transgenic G q overexpression induces cardiac contractile failure in mice

2. Calcineurin/NFAT Coupling Participates in Pathological, but not Physiological, Cardiac Hypertrophy

3. TRPC6 fulfills a calcineurin signaling circuit during pathologic cardiac remodeling

4. Calcineurin‐dependent cardiomyopathy is activated by TRPC in the adult mouse heart

5. TRPC3 and TRPC6 are essential for angiotensin II-induced cardiac hypertrophy

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