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骨硬化蛋白在骨关节炎发展中的作用:一篇综述。

Sclerostin in the development of osteoarthritis: A mini review.

作者信息

Chin K Y, Ekeuku S O, Pang K L

机构信息

Universiti Kebangsaan Malaysia, Faculty of Medicine, Department of Pharmacology, Kuala Lumpur, Malaysia.

Newcastle University Medicine Malaysia, Malaysia.

出版信息

Malays J Pathol. 2022 Apr;44(1):1-18.

Abstract

Wnt signalling plays an important role in bone and cartilage metabolism. Activation of Wnt signalling promotes bone formation but cartilage degradation. Sclerostin (SOST) can inhibit Wnt signalling. It is expressed by chondrocytes in the articular cartilage and osteocytes in the subchondral bone. Since osteoarthritis (OA) is a joint degenerative disease involving both bone and joint compartments, SOST may have a role in mediating the progression of this disease. This review examined the current literature on the role of SOST in the pathogenesis of OA and its usefulness as a biomarker of OA. Most studies agree that SOST is upregulated as a rescue mechanism in OA to prevent further degenerative changes of the joint. It antagonises inflammation-induced cartilage catabolism while preserving chondrocyte anabolic activities. It also prevents abnormal bone mineralisation and osteophyte formation. However, studies on the performance of SOST as a biomarker to detect and stage OA are limited. Further studies are required to determine whether SOST can be a biomarker or therapeutic target for OA.

摘要

Wnt信号通路在骨骼和软骨代谢中发挥着重要作用。Wnt信号通路的激活促进骨形成,但会导致软骨降解。硬化蛋白(SOST)可抑制Wnt信号通路。它由关节软骨中的软骨细胞和软骨下骨中的骨细胞表达。由于骨关节炎(OA)是一种涉及骨骼和关节腔室的关节退行性疾病,SOST可能在介导该疾病的进展中发挥作用。本综述研究了关于SOST在OA发病机制中的作用及其作为OA生物标志物的实用性的现有文献。大多数研究一致认为,SOST在OA中作为一种挽救机制被上调,以防止关节进一步发生退行性变化。它拮抗炎症诱导的软骨分解代谢,同时保留软骨细胞的合成代谢活性。它还可防止异常骨矿化和骨赘形成。然而,关于SOST作为检测和分期OA的生物标志物的性能的研究有限。需要进一步研究以确定SOST是否可以成为OA的生物标志物或治疗靶点。

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