Calcineurin Splicing Variant Calcineurin Aβ1 Improves Cardiac Function After Myocardial Infarction Without Inducing Hypertrophy | Zendy

Leanne E. Felkin | Zendy; Takuya Narita | Zendy; Renée Germack | Zendy; Yasunori Shintani | Zendy; Kunihiko Takahashi | Zendy; Padmini Sarathchandra | Zendy; Marina LópezOlañeta | Zendy; Jesús M. Gómez-Salinero | Zendy; Ken Suzuki | Zendy; Paul J.R. Barton | Zendy; Nadia Rosenthal | Zendy; Enrique LaraPezzi | Zendy

Open Access

Calcineurin Splicing Variant Calcineurin Aβ1 Improves Cardiac Function After Myocardial Infarction Without Inducing Hypertrophy

Author(s) -

Leanne E. Felkin,

Takuya Narita,

Renée Germack,

Yasunori Shintani,

Kunihiko Takahashi,

Padmini Sarathchandra,

Marina LópezOlañeta,

Jesús M. Gómez-Salinero,

Ken Suzuki,

Paul J.R. Barton,

Nadia Rosenthal,

Enrique LaraPezzi

Publication year - 2011

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.110.012211

Subject(s) - calcineurin , nfat , pi3k/akt/mtor pathway , protein kinase b , medicine , fibrosis , muscle hypertrophy , microbiology and biotechnology , proinflammatory cytokine , wortmannin , endocrinology , biology , signal transduction , inflammation , transplantation

Calcineurin is a calcium-regulated phosphatase that plays a major role in cardiac hypertrophy. We previously described that alternative splicing of the calcineurin Aβ (CnAβ) gene generates the CnAβ1 isoform, with a unique C-terminal region that is different from the autoinhibitory domain present in all other CnA isoforms. In skeletal muscle, CnAβ1 is necessary for myoblast proliferation and stimulates regeneration, reducing fibrosis and accelerating the resolution of inflammation. Its role in the heart is currently unknown.

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