REVIEW article
Front. Cell Dev. Biol.
Sec. Molecular and Cellular Pathology
Frontier Research on Mechanisms of Bone Destruction in Rheumatoid Arthritis
虹婷 卢 1
Niqin Xiao 2
Qianqian Yang 2
Yundong Xu 2
Jian Wang 2
Zhaohu Xie 2
Zhaofu Li 2
Heguo Yan 2
Xi Liu 2
Qiumei He 2
Kuanmeng Chi 2
Yuanyuan Wei 2
1. First Affiliated Hospital of Yunnan University of Traditional Chinese Medicine, Kunming, China
2. Yunnan Provincial Hospital of Chinese Medicine, Kunming, China
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Abstract
Progressive bone destruction in rheumatoid arthritis (RA) represents a core pathological mechanism leading to joint dysfunction. Its pathogenesis involves multiple critical pathways, including abnormal activation of immune and synovial cells, excessive proinflammatory cytokine secretion, and disrupted bone remodeling balance. Recent advancements in research techniques and academic exploration have progressively refined our understanding of RA-related bone destruction regulatory mechanisms. Programmed Cell Death (PCD), long non-coding RNAs (LncRNAs), and the significantly enhanced glycolytic metabolism observed in RA patients all mediate the onset and progression of RA bone destruction by targeting these pathological pathways. These findings collectively reveal a complex regulatory network intertwining cell demise processes, epigenetic regulation, and metabolic reprogramming. This not only deepens our understanding of the pathological mechanisms underlying RA bone destruction but also provides novel theoretical support and potential therapeutic targets for developing multi-targeted intervention strategies against this pathological process.
Summary
Keywords
bone destruction, Glycolysis, long non-coding RNA, programmed cell death, Rheumatoid arthritis
Received
28 November 2025
Accepted
19 February 2026
Copyright
© 2026 卢, Xiao, Yang, Xu, Wang, Xie, Li, Yan, Liu, He, Chi and Wei. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Zhaohu Xie; Zhaofu Li
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