Fibroblastos sinoviales

Elena Izquierdo , José Luis Pablos
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引用次数: 1

摘要

滑膜成纤维细胞(SF)或成纤维细胞样滑膜细胞是关节滑膜的主要常驻细胞成分。大量研究支持SF在类风湿关节炎(RA)发病机制中起重要作用的假设。在RA滑膜中,SF数量增加(增生)并表现出表型改变,在缺乏外部刺激的培养中持续存在。这些异常与特定信号通路的激活有关,这些信号通路促进细胞生长和多种因素的表达,如细胞因子、趋化因子、生长因子、粘附分子和基质降解酶。SF的激活和扩张似乎有助于炎症细胞的募集、保留和激活,新血管的形成(血管生成),以及骨和软骨的破坏。SF对这些过程的相对贡献在动物模型中非常重要,但由于缺乏专门针对这些细胞的治疗干预措施,在人类RA中尚未确定。识别与类风湿SF表型改变相关的分子通路及其病理生理作用是开发非靶向免疫系统的慢性炎症和关节损伤的新治疗方案的基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Fibroblastos sinoviales

Synovial fibroblasts (SF) or fibroblast-like synoviocytes are the major resident cellular component of joint synovial membrane. Numerous studies support the hypothesis that SF play an important role in the pathogenesis of rheumatoid arthritis (RA). In the RA synovial membrane, SF increase in number (hyperplasia) and exhibit an altered phenotype that persists in culture in the absence of external stimuli. These abnormalities are associated with the activation of specific signalling pathways that promote cell growth and the expression of multiple factors such as cytokines, chemokines, growth factors, adhesion molecules, and matrix degradation enzymes. The activation and expansion of SF appear to contribute to the recruitment, retention and activation of inflammatory cells, new blood vessel formation (angiogenesis), and bone and cartilage destruction. The relative contribution of SF to these processes is very important in animal models but has not been determined in human RA due to the lack of treatment interventions specifically targeting these cells. The identification of the molecular pathways involved in the altered phenotype of rheumatoid SF and their pathophysiological contribution are the basis for the development of new therapeutic alternatives for chronic inflammation and joint damage not targeting the immune system.

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