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氧化型低密度脂蛋白在骨关节炎发病机制中的作用:叙述性综述。

The role of oxidation of low-density lipids in pathogenesis of osteoarthritis: A narrative review.

机构信息

Department of Orthopaedic Surgery, Kindai University Hospital, Osaka-Sayama City, Osaka, Japan.

出版信息

J Int Med Res. 2020 Jun;48(6):300060520931609. doi: 10.1177/0300060520931609.

Abstract

Osteoarthritis (OA) is a chronic joint disorder that causes degeneration of cartilage, synovial inflammation, and formation of osteophytes. Aging, obesity, and sex are considered the main risk factors of OA. Recent studies have suggested that metabolic syndrome (MetS) disorders, such as hypertension, hyperlipidemia, diabetes mellitus, and obesity, may be involved in the pathogenesis and progression of OA. MetS disorders are common diseases that also result in atherosclerosis. Researchers believe that OA and atherosclerosis have underlying similar molecular mechanisms because the prevalence of both diseases increases with age. Oxidation of low-density lipoprotein (ox-LDL) is believed to play a role in the pathogenesis of atherosclerosis. Recent reports have shown that ox-LDL and low-density lipoprotein receptor 1 (LOX-1) are involved in the pathogenesis of OA. The purpose of this narrative review is to summarize the current understanding of the role of the LOX-1/ox-LDL system in the pathogenesis of OA and to reveal common underlying molecular pathways that are shared by MetS in OA and the LOX-1/ox-LDL system.

摘要

骨关节炎(OA)是一种慢性关节疾病,可导致软骨退化、滑膜炎症和骨赘形成。衰老、肥胖和性别被认为是 OA 的主要危险因素。最近的研究表明,代谢综合征(MetS)等疾病,如高血压、高血脂、糖尿病和肥胖,可能参与 OA 的发病机制和进展。MetS 疾病是常见疾病,也会导致动脉粥样硬化。研究人员认为 OA 和动脉粥样硬化有潜在的相似分子机制,因为这两种疾病的患病率都随年龄增长而增加。氧化型低密度脂蛋白(ox-LDL)被认为在动脉粥样硬化的发病机制中起作用。最近的报告显示,ox-LDL 和低密度脂蛋白受体 1(LOX-1)参与了 OA 的发病机制。本综述的目的是总结目前对 LOX-1/ox-LDL 系统在 OA 发病机制中的作用的认识,并揭示 MetS 在 OA 中与 LOX-1/ox-LDL 系统共同存在的常见潜在分子途径。

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