Chemokines in cartilage degradation
Chemokines in cartilage degradation
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DOI：
10.1097/01.blo.0000143805.64755.4f
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发表时间：
2004-10-01
影响因子：
4.2
通讯作者：
Facchini, A
中科院分区：
文献类型：
--
作者：
Borzì, RM;Mazzetti, I;Facchini, A
除了已知的典型炎性细胞因子（IL-1 β、TNF α）的活性外，最近还报道了趋化因子及其受体在骨关节炎软骨降解中的作用。人软骨细胞可以产生CC和CXC趋化因子，并表达两种趋化因子亚家族的趋化因子受体。这些受体的结合可以诱导基质降解酶如基质金属蛋白酶1、3和13以及N-乙酰基-β-D-氨基葡糖苷酶的释放。此外，GRO α，一种作用于CXCR 2的CXC趋化因子，可以激活软骨细胞中的凋亡途径，导致软骨细胞死亡。这些发现表明趋化因子可以作为软骨细胞上的自分泌或旁分泌环，并且可以促成骨关节炎中存在的许多病理生理模式。趋化因子及其下游信号通路可以被认为是骨关节炎的新的治疗靶点。
Besides the well-known activities of the prototypical inflammatory cytokines (IL-1beta, TNFalpha), a role for chemokines and their receptors in cartilage degradation in osteoarthritis has recently been reported. Human chondrocytes can produce CC and CXC chemokines and express chemokine receptors for both chemokine subfamilies. Engagement of these receptors can induce the release of matrix degrading enzymes such as matrix metalloproteinases 1, 3, and 13, and N-acetyl-beta-D-glucosaminidase. Furthermore GROalpha, a CXC chemokine acting on CXCR2, can activate an apoptotic pathway in chondrocytes that leads to chondrocyte cell death. These findings suggest that chemokines can act as an autocrine or paracrine loop on chondrocytes and can contribute to many pathophysiological patterns present in osteoarthritis. Chemokines and their downstream signaling pathways can be considered novel therapeutic targets in osteoarthritis.