RHOA and diabetes mellitus: The pathophysiology of diabetes-induced ED is multifactorial, and the proposed mechanisms include: elevated advanced glycation end-products, increased levels of oxygen free radicals, impaired nitric oxide synthesis, increased endothelin B receptor binding sites and up-regulated Ras homolog family member A (RhoA/Rho-kinase pathway), neuropathic damage and impaired cyclic guanosine monophosphate (cGMP)-dependent protein kinase-1 [4].