Identifying therapeutic strategies towards increasing resilience to heart disease and improving overall health and lifespan of patients
The heart can be stressed in various ways (developmental defects, hypertension, ischemia, chemotherapies, etc.), and myocardial tissue responds by remodeling to compensate and maintain cardiac output. The ability for cardiac cells to undergo cell fate transitions during myocardial remodeling underlies the dynamic resilience of the heart, with disruptions to these processes driving pathogenic remodeling and eventually leading to heart failure.
By using approaches ranging from murine models of heart disease to bioinformatic analyses of single cell transcriptomics, with translational clinical data analyses and mechanistic cell culture models, we are investigating cardiac interstitial cell fate transitions and underling mechanistic drivers of regenerative and pathogenic myocardial remodeling.
Current projects in the lab focus on cardiac microvascular remodeling, somatic mutations, and cardio-oncology. Our ultimate goal is to identify therapeutic strategies towards increasing resilience to heart disease and improving overall healthspan and lifespan of patients.