Cooke John P
Division of Cardiovascular Medicine, Stanford University, 300 Pasteur Drive, Falk CVRC, Stanford CA 94305-5406, United States.
Life Sci. 2007 May 30;80(24-25):2347-51. doi: 10.1016/j.lfs.2007.01.061. Epub 2007 Feb 17.
An endothelial nicotinic acetycholine receptor (nAChR) mediates endothelial proliferation, survival, migration and tube formation in vitro, and angiogenesis in vivo. Exogenous nicotine stimulates this angiogenic pathway. This action of nicotine may contribute to tumor angiogenesis and tumor growth; atherosclerotic plaque neovascularization and progression; and other tobacco-related diseases. The endothelial nAChR mediates an angiogenic pathway that is interdependent with growth factor mediated pathways, as shown by pharmacological and molecular studies. The characterization of this new angiogenic pathway may provide a new therapeutic avenue for disorders of insufficient or pathological angiogenesis.
内皮烟碱型乙酰胆碱受体(nAChR)在体外介导内皮细胞增殖、存活、迁移和管状结构形成,在体内介导血管生成。外源性尼古丁可刺激这一血管生成途径。尼古丁的这一作用可能促进肿瘤血管生成和肿瘤生长;动脉粥样硬化斑块新生血管形成和进展;以及其他与烟草相关的疾病。药理学和分子研究表明,内皮nAChR介导的血管生成途径与生长因子介导的途径相互依存。对这一新血管生成途径的特性描述可能为血管生成不足或病理性血管生成相关疾病提供新的治疗途径。