Abstract
Enhanced activity of Pyk2, a proline-rich tyrosine kinase sensitive to Ca2+ and reactive oxygen species (ROS), has been reported in human heart failure. However, exact role of Pyk2 in cardiac pathophysiology remains controversial, with both protective and deleterious effects on intracellular Ca2+ homeostasis have been previously demonstrated. To investigate the role of Pyk2 in cardiac arrhythmogenesis, we used rat model for cardiac hypertrophy, induced by thoracic aortic banding (TAB). Pyk2 activity was manipulated using specific Pyk2 inhibitor PF431396 and adenoviral-mediated expression of Pyk2-inhibiting peptide CRNK.
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