Heidenreich Regina, Röcken Martin, Ghoreschi Kamran
Department of Dermatology, University of Tübingen, University Medical Center, Tübingen, Germany.
Drug News Perspect. 2008 Mar;21(2):97-105. doi: 10.1358/dnp.2008.21.2.1188196.
Angiogenesis is a hallmark of chronic inflammation such as psoriasis. Unraveling the pathogenesis of psoriasis shows that several proangiogenic mediators are activated and highly expressed during psoriasis. Vascular endothelial growth factor, hypoxia- inducible factor, tumor necrosis factor, interleukin-8 and angiopoietins are considered to be the main players responsible for the strong vessel formation in psoriasis. The proangiogenic milieu in the skin seems to result from a proinflammatory immune response initiated by T helper cells. Interestingly, several small molecules as well as modern biologics used for systemic therapy of psoriasis have been shown to provide not only immune regulatory effects but also influence endothelial cell biology. Thus, direct targeting of angiogenesis may not only help to understand psoriasis pathogenesis but also to develop new strategies to treat psoriasis with therapeutics that halt the angiogenesis required for the inflammatory disease.
血管生成是银屑病等慢性炎症的一个标志。对银屑病发病机制的深入研究表明，在银屑病期间，几种促血管生成介质被激活并高度表达。血管内皮生长因子、缺氧诱导因子、肿瘤坏死因子、白细胞介素 - 8和血管生成素被认为是导致银屑病中强烈血管形成的主要因素。皮肤中的促血管生成环境似乎源于辅助性T细胞引发的促炎免疫反应。有趣的是，用于银屑病全身治疗的几种小分子以及现代生物制剂不仅具有免疫调节作用，还会影响内皮细胞生物学。因此，直接靶向血管生成不仅有助于理解银屑病的发病机制，还能开发新的治疗策略，使用能够阻止炎症性疾病所需血管生成的疗法来治疗银屑病。
