Abstract

Endothelium-derived nitric oxide (NO) plays a critical role in angiogenesis. The angiogenic effects of vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), and other growth factors are mediated to a significant degree by their stimulation of NO release. Angiogenic processes known to be dependent upon NO release include endothelial cell survival, proliferation, migration, and interaction with the extracellular matrix, as well as mobilization of endothelial progenitor cells from the bone marrow. Pharmacological inhibition or genetic disruption of the NO synthase pathway interfere with angiogenesis. Because it is a competitive antagonist of NO synthase, asymmetric dimethylarginine (ADMA) also acts as an endogenous inhibitor of angiogenesis. Conditions that increase plasma ADMA levels impair angiogenesis, whereas therapeutic measures to counteract the influence of ADMA enhance angiogenesis. Manipulation of ADMA generation or metabolism may represent a new therapeutic approach for angiogenesis-related disorders.

Original languageEnglish (US)
Pages (from-to)115-121
Number of pages7
JournalEuropean Journal of Clinical Pharmacology
Volume62
Issue number1
DOIs
StatePublished - Feb 2006

Keywords

  • Dimethylarginine dimethylaminohydrolase
  • Hypercholesterolemia
  • Nitric oxide synthase

ASJC Scopus subject areas

  • Pharmacology (medical)
  • Pharmacology, Toxicology and Pharmaceutics(all)

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