The DDAH/ADMA pathway in the control of endothelial cell migration and angiogenesis
The DDAH/ADMA pathway in the control of endothelial cell migration and angiogenesis
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DOI：
10.1042/bst0371243
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发表时间：
2009-12-01
影响因子：
3.9
通讯作者：
Wojciak-Stothard, Beata
中科院分区：
文献类型：
--
作者：
Fiedler, Lorna R.;Wojciak-Stothard, Beata
ADMA(不对称二甲基精氨酸)是一种心血管危险因素，也是一氧化氮合酶(NOS)的内源性抑制物。ADMA由二甲基精氨酸二甲氨基水解酶(DDAHs)代谢。ADMA水平在与异常血管生成相关的心血管疾病中升高，但其机制尚不清楚。最近的研究表明，改变ADMA在体内和体外的代谢可以调节Rho GTP酶的活性，Rho GTP酶是肌动蛋白动力学、内皮细胞运动和血管生成的关键调节因子。在目前的综述中，我们考虑了这一点以及其他依赖和不依赖NO的分子机制，即DDAH/ADMA途径调节血管生成的分子机制。
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.