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Nicotine and pathological angiogenesis.

机译：尼古丁和病理性血管生成。

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This paper describes the role of endothelial nicotinic acetylcholine receptors (nAChR) in diseases where pathological angiogenesis plays a role. An extensive review of the literature was performed, focusing on studies that investigated the effect of nicotine upon angiogenesis. Nicotine induces pathological angiogenesis at clinically relevant concentrations (i.e. at tissue and plasma concentrations similar to those of a light to moderate smoker). Nicotine promotes endothelial cell migration, proliferation, survival, tube formation and nitric oxide (NO) production in vitro, mimicking the effect of other angiogenic growth factors. These in vitro findings indicate that there may be an angiogenic component to the pathophysiology of major tobacco related diseases such as carcinoma, atherosclerosis, and age-related macular degeneration. Indeed, nicotine stimulates pathological angiogenesis in pre-clinical models of these disorders. Subsequently, it has been demonstrated that nicotine stimulates nAChRs on the endothelium to induce angiogenic processes, that these nAChRs are largely of the α7 homomeric type, and that there are synergistic interactions between the nAChRs and angiogenic growth factor receptors at the phosphoproteomic and genomic levels. These findings are of potential clinical relevance, and provide mechanistic insights into tobacco-related disease. Furthermore, these findings may lead to novel therapies for diseases characterized by insufficient or inappropriate angiogenesis.
机译：本文介绍了在病理性血管生成起作用的疾病中，内皮烟碱型乙酰胆碱受体（nAChR）的作用。进行了广泛的文献回顾，重点是研究尼古丁对血管生成的影响的研究。尼古丁在临床上相关的浓度下（即在组织和血浆中的浓度类似于轻度至中度吸烟者的浓度）诱导病理性血管生成。尼古丁在体外促进内皮细胞迁移，增殖，存活，管形成和一氧化氮（NO）产生，模仿其他血管生成生长因子的作用。这些体外发现表明，与烟草相关的主要疾病，例如癌，动脉粥样硬化和与年龄有关的黄斑变性的病理生理可能存在血管生成成分。实际上，在这些疾病的临床前模型中，尼古丁会刺激病理性血管生成。随后，已经证明尼古丁刺激内皮上的nAChRs诱导血管生成过程，这些nAChRs很大程度上是α7同源型，并且在磷酸化蛋白质组学和基因组水平上nAChRs与血管生成生长因子受体之间存在协同相互作用。这些发现具有潜在的临床意义，并提供了与烟草相关疾病的机理性见解。此外，这些发现可能导致针对以血管生成不足或不适当为特征的疾病的新疗法。

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