Key result
Focal adhesion kinase plays a critical role in the cellular responses of cardiomyocytes and cardiac fibroblasts to biomechanical stress and hypertrophic agonists in cardiac hypertrophy and failure.
FAK signaling is a critical mediator of cardiomyocyte and fibroblast responses to biomechanical stress and hypertrophic agonists in the pathophysiology of cardiac hypertrophy and failure.
FAK merits investigation as a therapeutic target in hypertrophy; leaves open clinical translation from mechanistic data.
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.
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Franchini et al. (2009) conducted a review in Cardiac hypertrophy and failure. Focal adhesion kinase (FAK) signaling was evaluated. Focal adhesion kinase plays a critical role in the cellular responses of cardiomyocytes and cardiac fibroblasts to biomechanical stress and hypertrophic agonists in cardiac hypertrophy and failure.
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