Effect of asymmetric dimethylarginine (ADMA) on heart failure development

Xiaoyu Liu, Lei Hou, Dachun Xu, Angela Chen, Liuqing Yang, Yan Zhuang, Yawei Xu, John T. Fassett, Yingjie Chen

Research output: Contribution to journalReview article

23 Scopus citations


Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthases that limits nitric oxide bioavailability and can increase production of NOS derived reactive oxidative species. Increased plasma ADMA is a one of the strongest predictors of mortality in patients who have had a myocardial infarction or suffer from chronic left heart failure, and is also an independent risk factor for several other conditions that contribute to heart failure development, including hypertension, coronary artery disease/atherosclerosis, diabetes, and renal dysfunction. The enzyme responsible for ADMA degradation is dimethylarginine dimethylaminohydrolase-1 (DDAH1). DDAH1 plays an important role in maintaining nitric oxide bioavailability and preserving cardiovascular function in the failing heart. Here, we examine mechanisms of abnormal NO production in heart failure, with particular focus on the role of ADMA and DDAH1.

Original languageEnglish (US)
Pages (from-to)73-81
Number of pages9
JournalNitric Oxide - Biology and Chemistry
StatePublished - Apr 1 2016


  • Asymmetric dimethylarginine
  • Dimethylarginine dimethylaminohydrolase-1
  • Heart failure
  • Nitric oxide

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