Dysregulation of H11 Kinase in the Failing Human Left Ventricular Myocardium

The failing human LV manifests increased H11K protein levels independent of HF etiology. The reduced H11K protein level in mitochondria and its increase in the cytosolic compartment of failing cardiomyocytes represents an adverse maladaptation capable of reducing ATP synthesis by mitochondria and activation of cardiomyocyte pro-apoptotic cell death pathways in the cytosol respectively thus likely contributing to the progression of HF.