Research Progress of Abnormal Glycosylation in Osteoarthritis

Abstract

Osteoarthritis is a common degenerative joint disease mainly caused by degenerative damage to articular cartilage and reactive hyperplasia of the marginal and subchondral bone of the joint, which seriously affects the quality of life of patients. In recent years, the role of glycosylation as a key post-translational modification of proteins in the occurrence and development of OA has received increasing attention. Abnormal glycosylation involves not only the accumulation of advanced glycation end products (AGEs), but also dysregulation of enzymatic glycosylation processes, both of which are involved in the pathological changes of joint multitissue, but the specific mechanisms have not been fully elucidated. This article aims to systematically explore the association between abnormal glycosylation and OA, with a focus on its mechanism of action in articular cartilage, synovial membrane and subchondral bone, and to review the research progress in recent years, with the aim of providing a new perspective for the mechanism study and treatment strategy of OA.