A requirement for integrin-mediated adhesion in cardiac physiology is revealed 
through targeted deletion of integrin-associated genes in the murine heart. Here 
we show that targeted ablation of the integrin-linked kinase (ILK) expression 
results in spontaneous cardiomyopathy and heart failure by 6 wk of age. Deletion 
of ILK results in disaggregation of cardiomyocytes, associated with disruption 
of adhesion signaling through the beta1-integrin/FAK (focal adhesion kinase) 
complex. Importantly, the loss of ILK is accompanied by a reduction in cardiac 
Akt phosphorylation, which normally provides a protective response against 
stress. Together, these results suggest that ILK plays a central role in 
protecting the mammalian heart against cardiomyopathy and failure.