Targeted focal adhesion kinase activation in cardiomyocytes protects the heart from ischemia/reperfusion injury.

ABSTRACT:

Objective

We previously reported that cardiac-restricted deletion of focal adhesion kinase (FAK) exacerbated myocyte death following ischemia/reperfusion (I/R). Here, we interrogated whether targeted elevation of myocardial FAK activity could protect the heart from I/R injury.

Methods and results

Transgenic mice were generated with myocyte-specific expression of a FAK variant (termed SuperFAK) that conferred elevated allosteric activation. FAK activity in unstressed transgenic hearts was modestly elevated, but this had no discernable effect on anabolic heart growth or cardiac function. Importantly, SuperFAK hearts exhibited a dramatic increase in FAK activity and a reduction in myocyte apoptosis and infarct size 24 to 72 hours following I/R. Moreover, serial echocardiography

SUBMITTER: Cheng Z 

PROVIDER: S-EPMC4237311 | biostudies-literature | 2012 Apr

REPOSITORIES: biostudies-literature