Key result
The DDAH/ADMA pathway regulates angiogenesis and endothelial cell motility through NO-dependent and -independent molecular mechanisms, including the modulation of Rho GTPases.
This review highlights the molecular mechanisms, including Rho GTPase modulation, by which the DDAH/ADMA pathway regulates endothelial cell migration and angiogenesis.
May inform endothelial-targeted therapies in vascular disease; leaves open clinical translation pending targeted trials.
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.
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Fiedler et al. (2009) conducted a review in Cardiovascular disorders associated with abnormal angiogenesis. DDAH/ADMA pathway was evaluated. The DDAH/ADMA pathway regulates angiogenesis and endothelial cell motility through NO-dependent and -independent molecular mechanisms, including the modulation of Rho GTPases.