Focal adhesion kinase and endothelial cell apoptosis

Focal adhesion kinase (FAK) is a key component of cell-substratum adhesions, known as focal adhesion complexes. Growing evidence indicates that FAK is important in maintenance of normal cell survival and that disruption of FAK signaling results in loss of substrate adhesion and anoikis (apoptosis) of anchorage-dependent cells, such as endothelial cells. Basal FAK activity in non-stimulated endothelial cells is important in maintaining cell adhesion to integrins via PI3 kinase/Akt signaling. FAK activity is dependent upon small GTPase signaling. FAK also appears to be important in cardiomyocyte hypertrophy and hypoxia/reoxygenation-induced cell death. This review summarizes the signaling pathways of FAK in prevention of apoptosis and the role of FAK in mediating adenosine and homocysteine-induced endothelial cell apoptosis and in cardiovascular diseases.

Research highlights
► Focal Adhesion Kinase (FAK) is important in maintenance of normal cell survival.
► FERM-mediated FAK translocation promotes cell survival via inhibition of p53.
► The tyrosine kinase activity of FAK is necessary for protection against apoptosis.
► FAK promotes cell survival via the PI3K/Akt pathway.