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Hypoxia and vitamin D differently contribute to leptin and dickkopf-related protein 2 production in human osteoarthritic subchondral bone osteoblasts

机译:低氧和维生素D对人骨关节炎软骨下成骨细胞中瘦素和与dickkopf相关的蛋白质2产生的贡献不同

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摘要

IntroductionBone remodelling and increased subchondral densification are important in osteoarthritis (OA). Modifications of bone vascularization parameters, which lead to ischemic episodes associated with hypoxic conditions, have been suspected in OA. Among several factors potentially involved, leptin and dickkopf-related protein 2 (DKK2) are good candidates because they are upregulated in OA osteoblasts (Obs). Therefore, in the present study, we investigated the hypothesis that hypoxia may drive the expression of leptin and DKK2 in OA Obs.
机译:简介骨重塑和软骨下致密化增加在骨关节炎(OA)中很重要。在OA中怀疑可能会导致导致与缺氧状态相关的缺血性发作的骨血管化参数的改变。在可能涉及的几个因素中,瘦素和与dickkopf相关的蛋白2(DKK2)是很好的候选者,因为它们在OA成骨细胞(Obs)中上调。因此,在本研究中,我们调查了缺氧可能驱动OA Obs中瘦素和DKK2表达的假说。

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