RHOA and coronary artery disorder: Ceconi et al. (2007) have also observed an increase on eNOS protein expression and activity in coronary artery disease patients treated with perindopril. It has been shown that NO may relieve vascular stiffness by inactivation of RhoA/Rho-kinase pathway through a cGMP-dependent protein kinase activation (Krepinsky et al., 2003; Sauzeau et al., 2003). In fact, NO has been considered the most powerful physiological endothelial relaxing factor that negatively regulates RhoA/Rho-kinase activation in the vasculature. For review, see Nunes and Webb (2020).