title: Asymmetric dimethylarginine and impaired cardiovascular healing.
abstract: Asymmetric dimethylarginine (ADMA) typically accumulates in the plasma of patients with chronic renal failure. Moreover, its plasma levels are raised in the presence of virtually all of the traditional cardiovascular risk factors. ADMA inhibits the three isoforms of nitric oxide (NO) synthase, thereby blunting the known cardioprotective effects of NO. Through its NO inhibitor actions, ADMA also exerts pro-apoptotic effects and suppresses progenitor cell mobilization, differentiation and function. Among patients with ischemic heart disease, low progenitor cell bioavailability and kidney dysfunction are emerging as strong predictors of death and recurrent cardiovascular events. We propose that patients with ischemic heart disease, kidney dysfunction, and high risk factor burden exhibit adverse cardiovascular outcomes, at least in part, through ADMA-mediated NO depression, enhanced apoptotic signalling, and reduced progenitor cell bioavailability, with consequent blunting of cardiovascular healing. Further research into the mechanisms that regulate the NO/ADMA balance may advance our understanding of cardiovascular diseases.
authors: Department of Cardiovascular Medicine, Catholic University Medical School, Rome, Italy. giucolu79@virgilio.it
authors: Giulio
authors: G
authors: Coluzzi
authors: Eleonora
authors: E
authors: Santucci
authors: Francesca
authors: F
authors: Marzo
authors: Felicita
authors: F
authors: Andreotti
mesh_terms: D017209:Apoptosis; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood; D002318:Cardiovascular Diseases; D006801:Humans; D007674:Kidney Diseases; D017202:Myocardial Ischemia; D009569:Nitric Oxide / Q000378:metabolism; D011379:Prognosis; D012038:Regeneration; D013234:Stem Cells; D016896:Treatment Outcome
chemical_list: D009569:Nitric Oxide; C018524:N,N-dimethylarginine; D001120:Arginine