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HSP75 protects against cardiac hypertrophy and fibrosis
Author(s) -
Zhang Yan,
Jiang DingSheng,
Yan Ling,
Cheng KuoJu,
Bian ZhouYan,
Lin GuoSheng
Publication year - 2011
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.23091
Subject(s) - muscle hypertrophy , pressure overload , medicine , fibrosis , protein kinase b , endocrinology , cardiac fibrosis , heart failure , phosphorylation , myocardial fibrosis , heat shock protein , cardiology , biology , cardiac hypertrophy , microbiology and biotechnology , gene , biochemistry
Cardiac hypertrophy, a major determinant of heart failure, is associated with heat shock proteins (HSPs). HSP75 has been reported to protect against environmental stresses; however, its roles in cardiac hypertrophy remain unclear. Here, we generated cardiac‐specific inducible HSP75 transgenic mice (TG) and cardiac hypertrophy was developed at 4 weeks after aortic banding in TG mice and wild‐type littermates. The results revealed that overexpression of HSP75 prevented cardiac hypertrophy and fibrosis as assessed by heart weight/body weight ratio, heart weight/tibia length ratio, echocardiographic and hemodynamic parameters, cardiomyocyte width, left ventricular collagen volume, and gene expression of hypertrophic markers. Further studies showed that overexpression of HSP75 inhibited the activation of TAK/P38, JNK, and AKT signaling pathways. Thus, HSP75 likely reduces the hypertrophy and fibrosis induced by pressure overload through blocking TAK/P38, JNK, and AKT signaling pathways. J. Cell. Biochem. 112: 1787–1794, 2011. © 2011 Wiley‐Liss, Inc.