PURPOSE: To understand the pathophysiology of diabetic erectile dysfunction (ED) and to review the current strategies against diabetic ED. MATERIALS AND METHODS: A systematic search was performed of MEDLINE databases to obtain articles pertaining to the pathophysiology and management of diabetic ED. RESULTS: No single etiology has been identified as the principal cause of ED. Studies from non-penile tissue have indicated hyperglycemia-induced mitochondrial superoxide production activates the four damaging pathways by inhibiting glyceraldehyde-3-phosphate dehydrogenase (GAPDH). It appears that these mechanisms provide molecular basis on which diabetes can affect erectile function by increasing reactive oxygen species, forming advanced glycation end products (AGEs) and activating protein kinase C pathway. Consequently, impaired vasorelaxation, enhanced vasoconstriction, nitrergic neural degeneration and structural and functional alteration of cavernosal integrity have been observed in subjects with diabetes. Furthermore, significant hypogonadism often exists in diabetic men, further complicating the understanding of diabetic ED. The treatment of diabetic ED is multimodal. Adequate control of hyperglycemia and comorbidities is prerequisite for the application of various treatments. The type 5 phosphodiesterase inhibitors (PDE5Is) are the mainstay of oral treatment of ED. Vacuum erection device and intracavernosal injection are still viable option when the treatment of PDE5I has failed. Patients with irreversible damage of the erectile mechanism are candidates for penile prosthesis implantation. Current concepts suggest that therapeutic prospects on the horizon include gene therapy, growth factor therapy and novel pharmacotherapies such as anti-AGE drugs. CONCLUSIONS: The current understading of diabetic ED is far from being satisfactory to offer adequate treatment. Future strategies in the evolution of the treatment of diabetic ED are aimed at correcting or treating underlying mechanisms.