Authors
Zewen Xu, Zhiwei Pei, Haobo Yang, Shanjie Guo, Qiang Li, Liuchang Jiang, Jing Wang, Leipeng Wang, Dexin Liu, Xuanyin Chen, Baoxin Zhang, Ting Hao
Published in
Journal of translational medicine. Jul 18, 2026. Epub Jul 18, 2026.
Abstract
Ribosomes are the core machinery for cellular protein synthesis, and defects in their biogenesis have been confirmed to be closely associated with various diseases. Osteoarthritis (OA), one of the most common joint diseases worldwide, has a complex pathogenesis that remains incompletely elucidated. Traditional research has primarily focused on metabolic imbalances in articular cartilage and inflammatory responses. However, growing evidence suggests that dysregulated ribosome biogenesis may play a critical role in the pathogenesis of OA. Impaired ribosome biogenesis limits the protein translation capacity of chondrocytes and may participate in the initiation and progression of OA by modulating cellular metabolism and stress responses, indicating that OA could be considered an acquired ribosomopathy.
This review systematically summarizes the various factors involved in ribosome biogenesis and their impact on chondrocyte function and joint tissue homeostasis, with a particular focus on key molecules such as non-coding RNAs, ribosomal proteins, and translation regulators. By integrating the latest findings from in vivo and in vitro models, this work evaluates the potential therapeutic value of targeting ribosome biogenesis-related molecules for the treatment of OA.
In summary, in-depth investigation of the role of ribosome biogenesis in OA may not only provide new perspectives for elucidating its pathological mechanisms but also offer a theoretical foundation and potential targets for developing therapeutic strategies that modify the disease course.
PMID:
42471720
Bibliographic data and abstract were imported from PubMed on 19 Jul 2026.
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