Department of Clinical Pharmacology and Therapeutics, BHF Laboratories, 5 University Street, Rayne Institute, University College London, London WC1E 6JJ, UK.
Biochem Soc Trans. 2009 Dec;37(Pt 6):1243-7. doi: 10.1042/BST0371243.
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.
精氨酸（ asymmetric dimethylarginine ，ADMA ）是心血管疾病的风险因子和一氧化氮合酶（ nitric oxide synthase ，NOS ）的内源性抑制剂。ADMA 由二甲基精氨酸二甲氨基水解酶（ dimethylarginine dimethylaminohydrolases ，DDAHs ）代谢。心血管疾病与异常血管生成有关，而 ADMA 水平在这些疾病中增加，但机制尚不清楚。最近的研究表明，改变体内和体外 ADMA 代谢可调节 Rho GTPases 的活性，而 Rho GTPases 是肌动蛋白动力学、内皮细胞迁移和血管生成的关键调节因子。在本综述中，我们考虑了 DDAH/ADMA 途径通过这种以及其他依赖和非依赖于一氧化氮的分子机制来调节血管生成。
