Enhancing Cardiac FAK Reduces Ischemia/Reperfusion Damage

Increased FAK activity confers protection via NF-κB pathway in mice

FRIDAY, March 2 (HealthDay News) -- Mice that overproduce focal adhesion kinase (FAK) experience less ischemia/reperfusion-induced apoptosis, according to a study published online March 1 in Arteriosclerosis, Thrombosis, and Vascular Biology.

Following up on previous results showing that deletion of FAK in the heart enhanced myocyte death in mice after ischemia and reperfusion, Zhaokang Cheng, Ph.D., and colleagues from the University of North Carolina at Chapel Hill, generated transgenic mice that produced excess levels of a FAK variant (SuperFAK) with increased activity in myocytes.

The researchers found that, after ischemia and reperfusion, the SuperFAK hearts had dramatic increases in FAK activity, with reduced myocyte death and infarct size within 24 to 72 hours. The mice were also protected from cardiac decompensation for up to eight weeks. Further investigation showed that the increased FAK activity conferred protection by activating the nuclear factor-κB (NF-κB) pathway during the early reperfusion period (30 and 60 minutes). In cultured cardiomyocytes, adenoviral-mediated expression of SuperFAK reduced the hypoxia/reoxygenation-induced apoptosis. The beneficial effect of SuperFAK was abolished by blockade of the NF-κB pathway via pharmacological inhibitor or small interfering RNAs.

"Enhancing cardiac FAK activity attenuates ischemia/reperfusion-induced myocyte apoptosis through activation of the prosurvival NF-κB pathway and may represent a novel therapeutic strategy for ischemic heart diseases," Cheng and colleagues conclude.

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