TRIM21 contributes to senile osteoporosis by shifting the osteoadipogenic balance toward adipogenesis in BMSCs.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

During aging, bone marrow stromal cells (BMSCs) tend to differentiate more into adipocytes than into osteoblasts, resulting in decreased bone formation and contributing to age-related osteoporosis and impaired bone regeneration. However, the molecular mechanisms underlying this process remain unclear. In this study, we observed an increase in the expression of TRIM21 in aged BMSCs, particularly those involved in adipogenesis. This increase in TRIM21 levels shifted the osteoadipogenic balance toward adipogenesis in BMSCs, resulting in reduced bone formation and ultimately leading to age-related osteoporosis and impaired bone regeneration. Mechanistically, activation of the IL-1β-JNK MAPK pathway triggered the expression of TRIM21 in aged BMSCs, which then shifted the osteoadipogenic balance toward adipogenesis by facilitating the degradation of β-catenin through K48 ubiquitination. Therefore, our findings suggest a potential intrinsic mechanism for age-related bone loss and suggest that targeting TRIM21 could be beneficial for treating age-related osteoporosis and impaired bone regeneration.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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