Physiological vascular smooth muscle cell plasticity is vital for vascular repair and homeostasis. At baseline, the tunica media of blood vessels is kept at an appropriate thickness, and vascular smooth muscle cells (VSMCs) have a quiescent, non-migratory contractile phenotype. Following vascular injury, these VSMCs are induced to dedifferentiate to a proliferative, migratory synthetic phenotype. Their growth and increased production of extracellular matrix (ECM) components result in a substantial thickening of the media and formation of a neointima. Followimg vascular repair and reestablishment of homeostasis, synthetic VSMCs are gradually induced to differentiate back to the contractile phenotype.