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ADMA (asymmetric dimethylarginine) is a cardiovascular risk factor and an endogenous inhibitor of NOS (nitric oxide synthase). ADMA is metabolized by DDAHs (dimethylarginine dimethylaminohydrolases). ADMA levels are increased in cardiovascular disorders associated with abnormal angiogenesis but the mechanisms are poorly understood. Recent studies show that altering ADMA metabolism in vivo and in vitro modulates the activity of Rho GTPases, key regulators of actin dynamics, endothelial cell motility and angiogenesis. In the present review, we consider this and other NO-dependent and -independent molecular mechanisms by which the DDAH/ADMA pathway regulates angiogenesis.

Original publication

DOI

10.1042/BST0371243

Type

Journal article

Journal

Biochem Soc Trans

Publication Date

12/2009

Volume

37

Pages

1243 - 1247

Keywords

Amidohydrolases, Animals, Apoptosis, Arginine, Cell Movement, Cell Proliferation, Endothelial Cells, Enzyme Inhibitors, Gene Expression Regulation, Developmental, Humans, Neovascularization, Physiologic, Nitric Oxide Synthase, Signal Transduction, Stem Cells, rho GTP-Binding Proteins