Our laboratory is interested in mechanisms governing pathological remodeling of the heart. Using molecular, physiological, and electrophysiological approaches, we study structural, functional, and electrical remodeling events occuring in heart disease. These studies are based on genetic and surgical models of heart disease in animals and cells in culture, as well as patients with hypertrophic heart disease and cardiomyopathy. Specific questions we are studying at present include:
- mechanisms governing the pathological growth response of the myocardium;
- autophagy as a novel mechanism of remodeling that contributes to the transition from stable hypertrophy to heart failure;
- FoxO transcription factors and their governance of cell growth, cell viability, autophagy, and protein degradation;
- mechanisms of Ca2+ metabolism in hypertrophied and failing ventricular myocytes with particular emphasis on transcriptional and post-translational regulation of the L-type Ca2+ channel;
- atrophic remodeling of the myocardium;
- stem cell-based therapy in heart disease, focusing on a niche of progenitor cells harbored within the ventricle, as well as exogenous, adipose tissue-derived progenitors.
