My research investigates the molecular mechanisms that drive pathological cardiac remodeling in the development of heart failure (HF). HF is a leading cause of illness and death worldwide, and projections show its burden continuing to grow, highlighting an urgent need for new therapies. Many stressors can trigger HF remodeling, including pressure overload, ischemic and metabolic stress, and genetic factors. My lab works to distinguish the adaptive responses to these stressors from the maladaptive ones, with the goal of designing targeted interventions that preserve adaptive response and prevent HF. Collectively, we study transcriptional and cytoskeletal regulatory mechanisms to address key aspects of heart physiology such as changes in cardiac dimensions, extracellular matrix remodeling and fibrosis, and electrical dysregulation and arrhythmia.