Molecular and cellular mechanisms of mechanical stress-induced cardiac hypertrophy

被引:26
作者
Zou, YZ [1 ]
Takano, H [1 ]
Akazawa, H [1 ]
Nagai, T [1 ]
Mizukami, M [1 ]
Komuro, I [1 ]
机构
[1] Chiba Univ, Grad Sch Med, Dept Cardiovasc Sci & Med, Chuo Ku, Chiba 2608670, Japan
关键词
mechanical stress; cardiac hypertrophy; signal transduction pathways;
D O I
10.1507/endocrj.49.1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Congestive heart failure is one of the major issues for cardiologists. Since cardiac hypertrophy deteriorates into heart failure, it is important to elucidate the mechanisms of cardiac hypertrophy. Hemodynamic overload, namely mechanical stress, is a major cause for cardiac hypertrophy. Mechanical stress induces various hypertrophic responses such as activation of phosphorylation cascades of many protein kinases, expression of specific genes and an increase in protein synthesis. During this process, secretion and production of vasoactive peptides such as angiotensin II and endothelin-1, are increased and play critical roles in the induction of these hypertrophic responses. Recently, a Ca2+ dependent protein kinase, CaMK, and a Ca2+ dependent protein phosphatase, calcineurin, have attracted great attention as critical molecules that induce cardiac hypertrophy. In this review, we described the mechanisms by which mechanical stress induces cardiac hypertrophy, especially focusing on the role of calcineurin in the development of cardiac hypertrophy.
引用
收藏
页码:1 / 13
页数:13
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