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.
Conference Article| November 19 2009
The DDAH/ADMA pathway in the control of endothelial cell migration and angiogenesis
Lorna R. Fiedler;
Beata Wojciak-Stothard 2
1Department of Clinical Pharmacology and Therapeutics, BHF Laboratories, 5 University Street, Rayne Institute, University College London, London WC1E 6JJ, U.K.
2To whom correspondence should be addressed, at the present address: Department of Experimental Medicine and Toxicology, Bulington Danes Building, Imperial College London, Du Cane Road, London W12 ONN, U.K. (email firstname.lastname@example.org).
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Lorna R. Fiedler, Beata Wojciak-Stothard; The DDAH/ADMA pathway in the control of endothelial cell migration and angiogenesis. Biochem Soc Trans 1 December 2009; 37 (6): 1243–1247. doi: https://doi.org/10.1042/BST0371243
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