Journal of Thrombosis and Thrombolysis

, Volume 27, Issue 2, pp 168–171

Asymmetric dimethylarginine and impaired cardiovascular healing

  • Giulio Coluzzi
  • Eleonora Santucci
  • Francesca Marzo
  • Felicita Andreotti
Article

DOI: 10.1007/s11239-007-0181-y

Cite this article as:
Coluzzi, G., Santucci, E., Marzo, F. et al. J Thromb Thrombolysis (2009) 27: 168. doi:10.1007/s11239-007-0181-y

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.

Keywords

Asymmetric dimethylarginineCardiovascular healing

Copyright information

© Springer Science+Business Media, LLC 2007

Authors and Affiliations

  • Giulio Coluzzi
    • 1
    • 2
    • 3
  • Eleonora Santucci
    • 1
  • Francesca Marzo
    • 1
  • Felicita Andreotti
    • 1
  1. 1.Department of Cardiovascular MedicineCatholic University Medical SchoolRomeItaly
  2. 2.NormaItaly
  3. 3.Department of Cardiovascular MedicineCatholic UniversityRomeItaly