Mingyu He, Jian Liu, Yanqiu Sun, Yanyan Fang, Fanfan Wang

Department of Rheumatology, the First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, Anhui Province, People’s Republic of China

Correspondence: Jian Liu, Department of Rheumatology, the First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, Anhui Province, People’s Republic of China, Tel +86 13955109537, Email liujianahzy@126.com

Abstract: 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.

Keywords: osteoarthritis, m6A, DNA methylation, pathogenesis, clinical treatment