Critical Role for Stromal Interaction Molecule 1 in Cardiac Hypertrophy
Author(s) -
JeanSébastien Hulot,
Jérémy Fauconnier,
Deepak Ramanujam,
Antoine H. Chaanine,
F. Cohen Aubart,
Yassine Sassi,
Sabine Merkle,
Olivier Cazorla,
Aude Ouillé,
Morgan Dupuis,
Lahouaria Hadri,
Dongtak Jeong,
Silke Mühlstedt,
Joachim P. Schmitt,
Attila Braun,
Ludovic Bénard,
Youakim Saliba,
Bernhard Laggerbauer,
Bernhard Nieswandt,
Alain Lacampagne,
Roger J. Hajjar,
AnneMarie Lompré,
Stefan Engelhardt
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.111.031229
Subject(s) - stim1 , muscle hypertrophy , medicine , in vivo , myocyte , microbiology and biotechnology , biology , endocrinology , chemistry , calcium
Cardiomyocytes use Ca2+ not only in excitation-contraction coupling but also as a signaling molecule promoting, for example, cardiac hypertrophy. It is largely unclear how Ca2+ triggers signaling in cardiomyocytes in the presence of the rapid and large Ca2+ fluctuations that occur during excitation-contraction coupling. A potential route is store-operated Ca2+ entry, a drug-inducible mechanism for Ca2+ signaling that requires stromal interaction molecule 1 (STIM1). Store-operated Ca2+ entry can also be induced in cardiomyocytes, which prompted us to study STIM1-dependent Ca2+ entry with respect to cardiac hypertrophy in vitro and in vivo.
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