MEF2B-Nox1 Signaling Is Critical for Stretch-Induced Phenotypic Modulation of Vascular Smooth Muscle Cells

These results suggest that CS initiates a signal through MEF2B that potentiates Nox1-mediated ROS production and causes VSMC to switch to a synthetic phenotype. The data also characterize a new Nox1 inhibitor as a potential therapy for treatment of vascular dysfunction in hypertension.