Novel Insights into the Regulatory Role of N6-Methyladenosine in the Pathogenesis and Clinical Treatment of Osteoarthritis: Research Status and Prospect

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)

Osteoarthritis (OA) is caused by characteristic joint tissue lesions characterized by chronic joint pain, stiffness, and limited mobility. OA is one of the most common causes of chronic disability in adults, seriously affecting the quality of life of patients and causing huge medical and socio-economic burdens. N6-methyladenosine (m6A) is a methylation that occurs at the N6 position of adenosine and is the most common chemical modification on eukaryotic RNA. m6A modification is a dynamic regulation process involving "writers" (methyltransferases), "erasers" (demethylases), and "readers" (reading proteins). Disruption or interference of this dynamic modification may lead to dysregulation of cellular regulatory mechanisms, resulting in various diseases. This article summarized the regulatory mechanism of m6A modification in OA pathogenesis, including regulation of inflammatory response and immune infiltration, extracellular matrix (ECM) degradation, programmed cell death, bone homeostasis, and osteogenic differentiation. Finally, the application and future development prospects of m6A modification in the clinical treatment of OA were further discussed.

Evidence level

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

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