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炎症性关节炎中骨损伤和修复的细胞和分子机制。

Cellular and molecular mechanisms of bone damage and repair in inflammatory arthritis.

机构信息

Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Botnar Research Centre, Oxford, UK.

Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Botnar Research Centre, Oxford, UK.

出版信息

Drug Discov Today. 2014 Aug;19(8):1178-85. doi: 10.1016/j.drudis.2014.06.025. Epub 2014 Jun 30.

DOI:10.1016/j.drudis.2014.06.025
PMID:24993158
Abstract

Bone remodelling relies on tightly controlled cycles of bone resorption and formation, mediated by osteoclasts and osteoblasts, respectively. The past two decades have seen a huge increase in our understanding of immune modulation and disruption of bone homeostasis in rheumatic diseases; identification of the molecular pathways responsible for accelerated bone loss in such conditions has given rise to potential novel therapeutic targets. Most recently, the role of microRNAs in inflammatory and noninflammatory bone loss raises the intriguing possibility that modification of cellular protein translation could also be a treatment strategy for bone damage.

摘要

骨重塑依赖于破骨细胞和成骨细胞分别介导的骨吸收和形成的紧密控制的循环。在过去的二十年中,我们对风湿性疾病中的免疫调节和骨稳态破坏有了深入的了解;确定了导致这些情况下骨丢失加速的分子途径,为潜在的新治疗靶点提供了依据。最近,microRNAs 在炎症性和非炎症性骨丢失中的作用提出了一个有趣的可能性,即细胞蛋白质翻译的修饰也可能是治疗骨损伤的一种策略。

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