Synovial inflammation in osteoarthritis progression.

Synovial inflammation in osteoarthritis progression.
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DOI:
10.1038/s41584-022-00749-9
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发表时间:
2022-05
期刊:
Nature reviews. Rheumatology
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其他
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骨关节炎(OA)是一种导致关节退变的进行性退行性疾病。滑膜炎症存在于OA关节中,并且与影像学表现和疼痛进展相关。包括衰老、肥胖、创伤和机械负荷在内的若干OA风险因素在OA发病机制中起作用,可能是通过改变滑膜生物学。此外,其他因素,如线粒体功能障碍、损伤相关分子模式、细胞因子、代谢物以及滑膜中的晶体,激活滑膜细胞并介导滑膜炎症。对参与OA相关滑膜炎症的激活途径的理解可以为患者分层和新型疗法的开发奠定基础。本综述重点关注OA滑膜的生物学,驻留在滑膜中或被招募到滑膜中的细胞如何相互作用,它们如何被激活,它们如何促进OA进展以及它们与其他关节结构的相互作用。
Osteoarthritis (OA) is a progressive degenerative disease resulting in joint deterioration. Synovial inflammation is present in the OA joint and has been associated with radiographic and pain progression. Several OA risk factors, including ageing, obesity, trauma and mechanical loading, play a role in OA pathogenesis, likely by modifying synovial biology. In addition, other factors, such as mitochondrial dysfunction, damage-associated molecular patterns, cytokines, metabolites and crystals in the synovium, activate synovial cells and mediate synovial inflammation. An understanding of the activated pathways that are involved in OA-related synovial inflammation could form the basis for the stratification of patients and the development of novel therapeutics. This Review focuses on the biology of the OA synovium, how the cells residing in or recruited to the synovium interact with each other, how they become activated, how they contribute to OA progression and their interplay with other joint structures.
滑膜巨噬细胞和巨噬细胞产生的细胞因子在驱动聚集蛋白聚糖酶、基质金属蛋白酶和骨关节炎中其他破坏性和炎症反应中的作用。
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