Homeostatic mechanisms in articular cartilage and role of inflammation in osteoarthritis.
Homeostatic mechanisms in articular cartilage and role of inflammation in osteoarthritis.
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DOI：
10.1007/s11926-013-0375-6
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发表时间：
2013-11
影响因子：
5
通讯作者：
Berenbaum, Francis
中科院分区：
文献类型：
--
作者：
Houard, Xavier;Goldring, Mary B.;Berenbaum, Francis
关键词：
骨关节炎（OA）是一种全关节疾病，其中软骨变薄和消失是OA进展的关键决定因素。软骨稳态的破裂，无论其原因是什么：衰老、遗传易感性、创伤或代谢紊乱，都会诱导软骨细胞的深刻表型改变，然后促进诱导软骨损伤和靶向其他关节组织的因子子集的合成。有趣的是，在这些因素中有许多炎症途径的组成部分。软骨细胞产生细胞因子、趋化因子、警报素、前列腺素类和脂肪因子，并表达细胞因子和趋化因子的多种细胞表面受体以及toll样受体。这些受体激活参与OA关节软骨细胞炎症和应激反应的细胞内信号通路。这篇综述着重于负责维持软骨稳态的机制，并强调了炎症过程在OA进展中的作用。
Osteoarthritis (OA) is a whole joint disease, in which thinning and disappearance of cartilage is a critical determinant in OA progression. The rupture of cartilage homeostasis whatever its cause: aging, genetic predisposition, trauma or metabolic disorder, induces profound phenotypic modifications of chondrocytes, which then promote the synthesis of a subset of factors that induce cartilage damage and target other joint tissues. Interestingly, among these factors are numerous components of the inflammatory pathways. Chondrocytes produce cytokines, chemokines, alarmins, prostanoids and adipokines and express numerous cell surface receptors for cytokines and chemokines, as well as toll-like receptors. These receptors activate intracellular signaling pathways involved in inflammatory and stress responses of chondrocytes in OA joints. This review focuses on mechanisms responsible for the maintenance of cartilage homeostasis and highlights the role of inflammatory processes in OA progression.
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