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首页> 外文期刊>Frontiers in bioscience: a journal and virtual library >Collagenase gene regulation by pro-inflammatory cytokines in cartilage
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Collagenase gene regulation by pro-inflammatory cytokines in cartilage

机译:软骨中促炎细胞因子对胶原酶基因的调控

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摘要

The essentially irreversible degradation of articular cartilage collagen represents a key, rate-limiting process in arthritic diseases. This process is typically initiated as a consequence of an inflammatory response, and if left unchecked ultimately leads to loss of joint function, pain, disability and a need for joint replacement surgery. Although we have identified the enzymes capable of effecting such destructive proteolysis, and considerable evidence indicates that tumour necrosis factor alpha and interleukin-1 are major pro-inflammatory mediators in joint destruction, we still know relatively little about how these mediators regulate collagenase gene expression in chondrocytes. Inflammatory arthritis has long been considered to be synovium-driven but compelling data now also implicate the chondrocyte, the sole cell type present in cartilage, as an active player in the destructive process. An understanding of how different cytokines interact, and how the pathways they activate cross-talk will not only provide important new insight into the mechanisms of joint destruction but also identify new targets for therapeutic intervention.
机译:关节软骨胶原蛋白的基本不可逆降解代表了关节炎疾病中的关键,限速过程。该过程通常是由于炎症反应而引发的,如果不加以控制,最终会导致关节功能丧失,疼痛,残疾和需要进行关节置换手术。尽管我们已经鉴定出能够实现这种破坏性蛋白水解的酶,并且大量证据表明肿瘤坏死因子α和白细胞介素1是关节破坏中的主要促炎介质,但对于这些介质如何调节胶原酶基因的表达,我们仍然知之甚少。软骨细胞。炎性关节炎长期以来一直被认为是滑膜驱动的,但令人信服的数据现在也表明软骨细胞是软骨中唯一的细胞类型,它是破坏过程中的活跃参与者。了解不同的细胞因子如何相互作用,以及它们如何激活串扰,不仅为关节破坏的机理提供了重要的新见解,而且还为治疗干预确定了新的靶点。

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