4.0 Article Proceedings Paper

NO and angiogenesis

Journal

ATHEROSCLEROSIS SUPPLEMENTS
Volume 4, Issue 4, Pages 53-60

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/S1567-5688(03)00034-5

Keywords

angiogenesis; asymmetric dimethylarginine; HMG coA reductase inhibition; L-arginine; NOS

Funding

  1. NCCIH NIH HHS [R01 AT/HL00204] Funding Source: Medline
  2. NHLBI NIH HHS [R01 HL-63685] Funding Source: Medline
  3. NIAID NIH HHS [P01AI50153] Funding Source: Medline
  4. NIA NIH HHS [P01 AG18784] Funding Source: Medline

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Angiogenesis requires the elaboration of endothelium-derived nitric oxide (NO). Angiogenic factors induce the release of NO from endothelial cells, which mediates a multiplicity of processes involved in angiogenesis. These NO-modulated processes include endothelial cell survival, proliferation, migration, and interaction with the extracellular matrix. Derangements of the NO synthase pathway impair angiogenesis. Accordingly, the competitive inhibitor of the NOS pathway asymmetric dimethylarginine (ADMA) acts as an endogenous inhibitor of angiogenesis. By contrast, agents which increase NO synthesis, such as low dose statins, enhance angiogenesis. Modulation of the NO synthase pathway could become a new therapeutic avenue for angiogenesis-related disorders. (C) 2003 Elsevier Ireland Ltd. All rights reserved.

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