Endothelial cells, fibroblasts and vasculitis.
Endothelial cells, fibroblasts and vasculitis.
复制标题
内皮细胞，成纤维细胞和血管炎。
DOI：
10.1093/rheumatology/keh542
复制
发表时间：
2005-07
期刊：
影响因子：
--
通讯作者：
Raza K
中科院分区：
文献类型：
--
作者：
Buckley CD;Rainger GE;Nash GB;Raza K
血管炎研究中最重要的问题之一不是为什么会发生血管炎症，而是为什么会以特定部位的方式持续存在。在这篇综述中，我们阐述了间质细胞，如成纤维细胞和周细胞，如何在调节血管炎发生的部位中发挥重要作用。平滑肌细胞和成纤维细胞直接影响上覆血管细胞的行为，放大内皮对促炎剂（如TNF-α）的反应，并允许增强和不适当的白细胞募集。因此，异常的局部血管间质环境可以影响局部内皮功能并驱动局部血管炎症的持续。然而，这种局部血管炎症可对全身血管系统产生远端影响，导致广泛的内皮细胞功能障碍。血管内皮功能障碍在一系列免疫介导的炎症性疾病中很常见，见于多个血管床，并且在诱导疾病缓解后是可逆的。驱动这种全身性血管内皮功能障碍的机制尚不清楚，但TNF-α和CRP等因素可能起作用。在全身性血管炎中持续存在这种广泛的内皮功能障碍似乎具有长期后果，导致动脉粥样硬化和过早缺血性心脏病的加速。它也可能是其他免疫介导的风湿性疾病（如类风湿关节炎）加速动脉粥样硬化的基础。
One of the most important questions in vasculitis research is not why inflammation of blood vessels occurs but why it persists, often in a site-specific manner. In this review we illustrate how stromal cells, such as fibroblasts and pericytes, might play an important role in regulating the site at which vasculitis occurs. Smooth muscle cells and fibroblasts directly influence the behaviour of overlying vascular cells, amplifying the response of the endothelium to proinflammatory agents such as TNF-α and allowing enhanced and inappropriate leucocyte recruitment. An abnormal local vascular stromal environment can therefore influence local endothelial function and drive the persistence of local vascular inflammation. However, such local vascular inflammation can have distant effects on the systemic vascular system, leading to widespread endothelial cell dysfunction. Vascular endothelial dysfunction is common in a range of immune-mediated inflammatory diseases, is seen in multiple vascular beds, and is reversible following the induction of disease remission. The mechanisms that drive such systemic vascular endothelial dysfunction are unclear but factors such as TNF-α and CRP may play a role. Persistence of such widespread endothelial dysfunction in systemic vasculitis appears to have long-term consequences, leading to the acceleration of atherosclerosis and premature ischaemic heart disease. It may also underlie the accelerated atherosclerosis seen in other immune-mediated rheumatic diseases, such as rheumatoid arthritis.
登录
查看更多内容
影响因子：
14.5
作者：
Ahmad, SA;Jung, YD;Ellis, LM
通讯作者：
Ellis, LM
DOI：
10.1073/pnas.1434429100
发表时间：
2003-09-16
影响因子：
11.1
作者：
Chi, JT;Chang, HY;Brown, PO
通讯作者：
Brown, PO
影响因子：
27.4
作者：
Filer, AD;Gardner-Medwin, JM;Bacon, PA
通讯作者：
Bacon, PA
影响因子：
16.8
作者：
Buckley, CD;Pilling, D;Salmon, M
通讯作者：
Salmon, M
影响因子：
10.8
作者：
Lai, PFH;Mohamed, F;Stewart, DJ
通讯作者：
Stewart, DJ