Open AccessIn vivo cardiac role of migfilin during experimental pressure overload
Author(s) -
Bernhard J. Haubner,
Daniel Moik,
Thomas Schuetz,
Martin F. Reiner,
Jakob Voelkl,
Katrin Streil,
Kerstin Bader,
Lei Zhao,
Claudia Scheu,
Johannes Mair,
Otmar Pachinger,
Bernhard Metzler
Publication year - 2015
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/cvv125
Subject(s) - pressure overload , in vivo , cardiac function curve , microbiology and biotechnology , medicine , serum response factor , cytoskeleton , gene expression , transcription factor , reprogramming , chemistry , biology , cardiology , gene , heart failure , cell , cardiac hypertrophy , biochemistry , genetics
Increased myocardial wall strain triggers the cardiac hypertrophic response by increasing cardiomyocyte size, reprogramming gene expression, and enhancing contractile protein synthesis. The LIM protein, migfilin, is a cytoskeleton-associated protein that was found to translocate in vitro into the nucleus in a Ca(2+)-dependent manner, where it co-activates the pivotal cardiac transcription factor Csx/Nkx2.5. However, the in vivo role of migfilin in cardiac function and stress response is unclear.
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