Suppr超能文献

类风湿关节炎中骨质流失的发病机制。

Pathomechanisms of bone loss in rheumatoid arthritis.

作者信息

Sakthiswary Rajalingham, Uma Veshaaliini Rajeswaran, Chin Kok-Yong, Das Srijit, Sirasanagandla Srinivasa Rao

机构信息

Department of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, Malaysia.

Department of Pharmacology, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, Malaysia.

出版信息

Front Med (Lausanne). 2022 Aug 17;9:962969. doi: 10.3389/fmed.2022.962969. eCollection 2022.

Abstract

Rheumatoid arthritis (RA) is an autoimmune disease, in which the inflammatory processes involve the skeletal system and there is marked destruction of the bones and the surrounding structures. In this review, we discuss the current concepts of osteoimmunology in RA, which represent the molecular crosstalk between the immune and skeletal systems, resulting in the disruption of bone remodeling. Bone loss in RA can be focal or generalized, leading to secondary osteoporosis. We have summarized the recent studies of bone loss in RA, which focused on the molecular aspects, such as cytokines, autoantibodies, receptor activator of nuclear kappa-β ligand (RANKL) and osteoprotegerin (OPG). Apart from the above molecules, the role of aryl hydrocarbon receptor (Ahr), which is a potential key mediator in this process through the generation of the Th17 cells, is discussed. Hence, this review highlights the key insights into molecular mechanisms of bone loss in RA.

摘要

类风湿关节炎(RA)是一种自身免疫性疾病,其炎症过程累及骨骼系统,骨骼及周围结构会出现明显破坏。在本综述中,我们讨论了RA中骨免疫学的当前概念,该概念代表了免疫和骨骼系统之间的分子相互作用,导致骨重塑紊乱。RA中的骨质流失可以是局部的或全身性的,会导致继发性骨质疏松症。我们总结了近期关于RA中骨质流失的研究,这些研究聚焦于分子层面,如细胞因子、自身抗体、核因子κB受体活化因子配体(RANKL)和骨保护素(OPG)。除上述分子外,还讨论了芳烃受体(Ahr)的作用,它通过产生Th17细胞,在此过程中可能是一个关键介质。因此,本综述突出了对RA中骨质流失分子机制的关键见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ade1/9428319/8665f91a0e85/fmed-09-962969-g0001.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验