Focal adhesion kinase signaling in cardiac hypertrophy and failure

被引:12
|
作者
Franchini, K. G. [1 ]
Clemente, C. F. M. Z. [1 ]
Marin, T. M. [1 ]
机构
[1] Univ Estadual Campinas, UNICAMP, Fac Ciencias Med, Dept Clin Med, BR-13083970 Campinas, SP, Brazil
基金
巴西圣保罗研究基金会;
关键词
Focal adhesion kinase; Mechanical signaling; Cardiovascular system; Signal transduction; TUBEROUS SCLEROSIS COMPLEX-2; TYROSINE-PHOSPHATASE SHP-2; PRESSURE-OVERLOAD; TERMINAL DOMAIN; HEART-FAILURE; PHOSPHORYLATION; ACTIVATION; FAK; INTEGRIN; EXPRESSION;
D O I
10.1590/S0100-879X2009000100008
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Focal adhesion kinase (FAK) is a broadly expressed tyrosine kinase implicated in cellular functions such as migration, growth and survival. Emerging data support a role for FAK in cardiac development, reactive hypertrophy and failure. Data reviewed here indicate that FAK plays a critical role at the cellular level in the responses of cardiomyocytes and cardiac fibroblasts to biomechanical stress and to hypertrophic agonists such as angiotensin II and endothelin. The signaling mechanisms regulated by FAK are discussed to provide insight into its role in the pathophysiology of cardiac hypertrophy and failure.
引用
收藏
页码:44 / 52
页数:9
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