Induction of intracellular heat-shock protein 72 prevents the development of vascular smooth muscle cell calcification
Author(s) -
Tzongshi Lu,
Kenneth Lim,
Guerman Molostvov,
YunChun Yang,
SzuYu Yiao,
Daniel Zehnder,
LiLi Hsiao
Publication year - 2012
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/cvs278
Subject(s) - heat shock protein , vascular smooth muscle , myocardin , gene knockdown , calcification , medicine , myocyte , pathogenesis , biology , microbiology and biotechnology , endocrinology , cancer research , gene expression , gene , serum response factor , biochemistry , smooth muscle
Vascular calcification (VC) is a significant contributor to cardiovascular mortality in patients with chronic kidney disease (CKD) and coronary artery disease (CAD). Osteo/chondrocytic transformation and simultaneous dedifferentiation of smooth muscle cells (SMCs) are important in the pathogenesis of VC. Heat-shock protein 72 (HSP72) is a cardioprotective inducible heat-shock protein that functions as a molecular chaperone. However, its role in the development of accelerated vascular dysfunction and calcification is largely unexplored.
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