Abstract
Endothelial-to-mesenchymal transition (EndoMT) is a form of cellular transdifferentiation essential for cardiovascular development but now recognized as a driver of vascular dysfunction in numerous adult diseases. It is also increasingly appreciated as a mechanistic link between endothelial injury, fibrosis, and immune dysregulation observed in many of these pathologies. However, the exact events leading up to the induction and maintenance of EndoMT remain the subject of continued research. In this review, we discuss the numerous triggers of EndoMT identified to date as well as the pathways contributing to a persistent mesenchymal phenotype. Potential future directions are highlighted with an eye toward pharmacologic reversal of EndoMT and restoration of endothelial function.