Asymmetric dimethylarginine: A key player in the pathophysiology of endothelial dysfunction, vascular inflammation and atherosclerosis in rheumatoid arthritis?

Arduino A. Mangoni, Sara Tommasi, Salvatore Sotgia, Angelo Zinellu, Panagiotis Paliogiannis, Matteo Piga, Alberto Cauli, Gianfranco Pintus, Ciriaco Carru, Gian L. Erre

Research output: Contribution to journalReview articlepeer-review

2 Citations (Scopus)

Abstract

Patients with rheumatoid arthritis (RA), a chronic and disabling autoimmune condition that is characterized by articular and extra-articular manifestations and a pro-inflammatory and pro-oxidant state, suffer from premature atherosclerosis and excessive cardiovascular disease burden. A key step in the pathogenesis of atherosclerosis is impaired synthesis of the endogenous messenger nitric oxide (NO) by endothelial cells which, in turn, alters local homeostatic mechanisms and favors vascular damage and plaque deposition. While the ex-act mechanisms of endothelial dysfunction in RA remain to be established, there is good evidence that RA patients have relatively high circulating concentrations of the methylated arginine asymmetric dimethylarginine (ADMA), a potent endogenous inhibitor of endothelial NO synthase (eNOS). This review discusses the biological and pathophysiological role of ADMA, the interplay between ADMA, inflammation and oxidative stress, and the available evidence on the adverse impact of ADMA on endothelial function and atherosclerosis and potential ADMA-lowering therapies in RA patients.

Original languageEnglish
Pages (from-to)2131-2140
Number of pages10
JournalCURRENT PHARMACEUTICAL DESIGN
Volume27
Issue number18
DOIs
Publication statusPublished - 2021

Keywords

  • Arterial stiffness
  • Asymmetric dimethylarginine
  • Atherosclerosis
  • Cardiovascular risk
  • Endothelial function
  • Inflammation
  • Rheumatoid arthritis

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