Adult mammalian hearts lack the ability to regenerate, and instead, respond to injury with maladaptive remodeling that leads to heart failure. In contrast, the newborn mouse heart can effectively regrow the damaged tissue. My lab will leverage single-cell genomic approaches, in vivo injury models, and mouse genetics to understand how cardiac cells respond to injury to regulate heart regeneration in neonates, with the ultimate goal of targeting gene transcription for regenerative medicine. Specifically, we will explore how injury-induced extrinsic cues act on cardiomyocytes to regulate proliferation and migration, and the role of transcriptional regulation in cardiac cell state transitions following injury. Answering these questions holds promise for unlocking the regeneration potential of human hearts.