Format

Send to

Choose Destination
Microvasc Res. 2012 Jan;83(1):56-63. doi: 10.1016/j.mvr.2011.05.003. Epub 2011 May 19.

Focal adhesion kinase and endothelial cell apoptosis.

Author information

1
Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, RI 02908, USA.

Abstract

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.

PMID:
21624380
PMCID:
PMC3189508
DOI:
10.1016/j.mvr.2011.05.003
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center