Muscle contraction is defined by the cyclical interaction between actin and myosin, an association primarily governed by the troponin complex in cardiac muscles. During pathophysiological conditions, efficient regulation of muscle contraction may be compromised by changes in the post-translational state and function of the contractile proteins or by alterations in the upstream signaling pathways that serve to modulate myocardial contractility.

Our laboratory is interested in examining the biophysical mechanism of cardiac muscle contraction under normal and pathophysiological states, as well as defining altered second messenger signaling pathways that modulate the protein-protein interactions governing the allosteric mechanism of regulation in cardiac muscles.