The main focus of the lab is the differentiated smooth muscle cell, which forms the walls of most of the hollow organs in the body. Inappropriate contraction or relaxation of smooth muscle is responsible for a number of diseases including stroke, hypertension, heart failure, asthma and premature labor.
We have had a longstanding interest in the differentiated smooth muscle cell. We are currently focused on the vascular cells in the aorta. The proximal aorta normally functions as a critical shock absorber to prevent the full force of the heartbeat from reaching the delicate small blood vessels of the brain, kidney, and heart, where it would cause damage and lead to dementia, kidney failure and heart failure. This shock absorber function is impaired with age. Thus aortic stiffness is both an early biomarker of, and a contributor to, adverse aging-related cardiovascular outcomes. We have identified specific cytoskeletal protein-protein interfaces as being involved in aging-induced increased aortic stiffness in a mouse model.
Our current efforts are focused on developing targeted potential therapeutic molecules to prevent or reverse the effects of aging on aortic stiffness and its consequent adverse cardiovascular and cognitive outcomes.