Open AccessProfilin modulates sarcomeric organization and mediates cardiomyocyte hypertrophy
Author(s) -
Viola Kooij,
Meera Viswanathan,
Dong I. Lee,
Peter P. Rainer,
William M. Schmidt,
William A. Kronert,
Siân E. Harding,
David A. Kass,
Sanford I. Bernstein,
Jennifer E. Van Eyk,
Anthony Cammarato
Publication year - 2016
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvw050
Subject(s) - profilin , actin , muscle hypertrophy , microbiology and biotechnology , cytoskeleton , actin cytoskeleton , biology , mediator , actin remodeling , cardiac hypertrophy , medicine , endocrinology , cell , genetics
Heart failure is often preceded by cardiac hypertrophy, which is characterized by increased cell size, altered protein abundance, and actin cytoskeletal reorganization. Profilin is a well-conserved, ubiquitously expressed, multifunctional actin-binding protein, and its role in cardiomyocytes is largely unknown. Given its involvement in vascular hypertrophy, we aimed to test the hypothesis that profilin-1 is a key mediator of cardiomyocyte-specific hypertrophic remodelling.
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