Kofler Sieglinde, Nickel Thomas, Weis Michael
Department of Cardiology, University Hospital Munich-Grosshadern, Ludwig-Maximilians University of Munich, 81377 Munich, Germany.
Clin Sci (Lond). 2005 Mar;108(3):205-13. doi: 10.1042/CS20040174.
Complex cellular and inflammatory interactions are involved in the progress of vascular diseases. Endothelial cells, upon exposure to cytokines, undergo profound alterations of function that involve gene expression and de novo protein synthesis. The functional reprogramming of endothelial cells by cytokines is of importance especially in patients with chronic vascular inflammation. The intercellular network of dendritic cells, T-lymphocytes, macrophages and smooth muscle cells generates a variety of stimulatory cytokines [e.g. TNF-alpha (tumour necrosis factor-alpha), IL (interleukin)-1, IL-6 and IFN-gamma (interferon-gamma)] and growth factors that promote the development of functional and structural vascular changes. High concentrations of proinflammatory cytokines increase oxidative stress, down-regulate eNOS (endothelial nitric oxide synthase) bioactivity and induce endothelial cell apoptosis. Chemoattractant cytokines [e.g. VEGF (vascular endothelial growth factor), TGF-beta1 (transforming growth factor-beta1) and IL-8] are important regulators of inflammation-induced angiogenesis and are directly modulated by nitric oxide. This review will focus on the vascular mechanisms orchestrated by cytokines and summarizes the current knowledge concerning the contribution of cytokines to cardiovascular diseases.
复杂的细胞和炎症相互作用参与了血管疾病的进展。内皮细胞在接触细胞因子后，会发生涉及基因表达和从头蛋白质合成的功能深刻改变。细胞因子对内皮细胞的功能重编程尤为重要，尤其是在慢性血管炎症患者中。树突状细胞、T淋巴细胞、巨噬细胞和平滑肌细胞的细胞间网络产生多种刺激细胞因子[如肿瘤坏死因子-α（TNF-α）、白细胞介素（IL）-1、IL-6和干扰素-γ（IFN-γ）]以及促进血管功能和结构变化发展的生长因子。高浓度的促炎细胞因子会增加氧化应激，下调内皮型一氧化氮合酶（eNOS）的生物活性并诱导内皮细胞凋亡。趋化性细胞因子[如血管内皮生长因子（VEGF）、转化生长因子-β1（TGF-β1）和IL-8]是炎症诱导血管生成的重要调节因子，并直接受一氧化氮调节。本综述将聚焦于细胞因子所调控的血管机制，并总结当前有关细胞因子对心血管疾病作用的知识。
