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Updated: Jan 16, 2026

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
Published on: March 18, 2022
HNRNPA1 promotes TRIM37 mRNA stability and mediates TRAF6 ubiquitination to alleviate osteoarthritis
Hailin Deng1, Wanlan Liu1, Liang Xiang1
1The Affiliated Nanhua Hospital, Department of Sports Medcine, Hengyang Medical School, University of South China, Hengyang 421002, Hunan, China.
Background:
Osteoarthritis (OA), characterized by progressive cartilage degeneration, involves inflammation and dysregulated cell death. The functional role of the RNA-binding protein HNRNPA1 via TRIM37-mediated TRAF6 ubiquitination in OA pathogenesis remains unclear.
Methods:
Using a destabilization of the medial meniscus (DMM)-induced OA mouse model, we assessed cartilage histopathology, inflammation, and expression of HNRNPA1, TRIM37, and TRAF6. Interleukin-1β (IL-1β)-treated chondrocytes were analyzed for viability, apoptosis, pyroptosis, and extracellular matrix (ECM) synthesis. Mechanistic studies included RNA-fluorescence in situ hybridization (RNA-FISH), RNA immunoprecipitation (RIP), mRNA stability assays, and co-immunoprecipitation (Co-IP) following TRIM37 knockdown to examine TRAF6 ubiquitination.
Results:
OA progression correlated with decreased HNRNPA1 and TRIM37 but increased TRAF6 expression. HNRNPA1 overexpression mitigated cartilage degradation, inflammation, and autophagy impairment. Mechanistically, HNRNPA1 stabilized TRIM37 mRNA, thereby enhancing TRIM37-mediated TRAF6 ubiquitination. This cascade suppressed pyroptosis while activating autophagy, conferring chondroprotection.
Conclusion:
The HNRNPA1/TRIM37/TRAF6 axis regulates the balance between autophagy and pyroptosis, offering a novel therapeutic target to alleviate OA.
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