Cooke John P
Program in Vascular Medicine and Biology, Stanford University School of Medicine, 300 Pasteur Dr., Stanford, CA 94305-5406, USA.
Atheroscler Suppl. 2003 Dec;4(4):53-60. doi: 10.1016/s1567-5688(03)00034-5.
Angiogenesis requires the elaboration of endothelium-derived nitric oxide (NO). Angiogenic factors induce the release of NO from endothelial cells, which mediates a multiplicity of processes involved in angiogenesis. These NO-modulated processes include endothelial cell survival, proliferation, migration, and interaction with the extracellular matrix. Derangements of the NO synthase pathway impair angiogenesis. Accordingly, the competitive inhibitor of the NOS pathway asymmetric dimethylarginine (ADMA) acts as an endogenous inhibitor of angiogenesis. By contrast, agents which increase NO synthesis, such as low dose statins, enhance angiogenesis. Modulation of the NO synthase pathway could become a new therapeutic avenue for angiogenesis-related disorders.
血管生成需要内皮衍生的一氧化氮(NO)的精细调控。血管生成因子诱导内皮细胞释放NO,其介导血管生成过程中涉及的多种进程。这些由NO调节的进程包括内皮细胞存活、增殖、迁移以及与细胞外基质的相互作用。NO合酶途径的紊乱会损害血管生成。因此,NOS途径的竞争性抑制剂不对称二甲基精氨酸(ADMA)作为血管生成的内源性抑制剂发挥作用。相比之下,增加NO合成的药物,如低剂量他汀类药物,可促进血管生成。调节NO合酶途径可能成为治疗血管生成相关疾病的新途径。