Our research extrapolates our understanding of embryonic heart development to inform strategies to enhance the inadequate regenerative capacity of the adult mammalian heart following myocardial infarction, with a particular focus on stimulating neovascularisation. Following injury, there is a partial recapitulation of embryonic processes that drive coronary vessel growth, yet fundamental differences in the regulatory pathways limit the efficacy of the adult response. Comparative analyses allow us to identify key mechanisms that may be targeted in the adult mammalian heart to enhance repair. Our research in murine models is complemented with the use of human iPSC-derived models of coronary vascular development.