Research in the Lincoln Lab is focused on understanding the molecular mechanisms that regulate normal heart formation in the embryo and identifying developmental origins of adult cardiovascular disease. More specifically, we are interested in examining the etiology of heart valve disease and examining parallels between valve development, and pathogenesis and regeneration of adult valves.
The formation of heart valves is a complex process involving multiple molecular pathways that modulate growth and morphogenesis of delicate, and highly organized leaflets. Alterations in these genetic networks during valvulogenesis frequently lead to congenital valve defects present at birth, including bicuspid aortic valve in 1-2% of the population. In addition to developmental defects, valve disease can be acquired and complications such as myxomatous degeneration and calcification are thought to arise from age-related ‘wear-and-tear’.
Despite the clinical significance, the regulatory pathways required for normal heart valve development and adult maintenance are largely unknown, and therefore we are unable to explain the etiology of congenital and acquired valve defects. To address this, my laboratory has established sophisticated tools to examine the molecular regulation of these processes in elegant model systems. Our long-term goal is to define the pathophysiology of heart valve disease and utilize these findings to develop alternative therapeutic strategies beyond surgical intervention.