Department of Vascular Biology and Inflammation, Centro Nacional de Investigaciones Cardiovasculares, Melchor Fernández Almagro 3, Madrid 28029, Spain.
Cardiovasc Res. 2010 May 1;86(2):226-35. doi: 10.1093/cvr/cvq049. Epub 2010 Feb 12.
Inflammation and angiogenesis are frequently coupled in pathological situations such as atherosclerosis, diabetes, and arthritis. The inflammatory response increases capillary permeability and induces endothelial activation, which, when persistent, results in capillary sprouting. This inflammation-induced angiogenesis and the subsequent remodelling steps are in large part mediated by extracellular matrix (ECM) proteins and proteases. The focal increase in capillary permeability is an early consequence of inflammation, and results in the deposition of a provisional fibrin matrix. Subsequently, ECM turnover by proteases permits an invasive program by specialized endothelial cells whose phenotype can be regulated by inflammatory stimuli. ECM activity also provides specific mechanical forces, exposes cryptic adhesion sites, and releases biologically active fragments (matrikines) and matrix-sequestered growth factors, all of which are critical for vascular morphogenesis. Further matrix remodelling and vascular regression contribute to the resolution of the inflammatory response and facilitate tissue repair.
在动脉粥样硬化、糖尿病和关节炎等病理情况下，炎症和血管生成经常同时发生。炎症反应会增加毛细血管通透性并诱导内皮细胞活化，持续的炎症反应会导致毛细血管出芽。这种炎症诱导的血管生成以及随后的重塑步骤在很大程度上是由细胞外基质 (ECM) 蛋白和蛋白酶介导的。毛细血管通透性的局部增加是炎症的早期后果，导致临时纤维蛋白基质的沉积。随后，蛋白酶对 ECM 的分解代谢允许专门的内皮细胞进行侵袭性程序，其表型可以受到炎症刺激的调节。ECM 活性还提供特定的机械力，暴露隐蔽的粘附位点，并释放生物活性片段（基质细胞衍生因子）和基质隔离的生长因子，所有这些对于血管形态发生都是至关重要的。进一步的基质重塑和血管退化有助于炎症反应的解决，并促进组织修复。
