Epigenetic modification and exosome effects on autophagy in osteoarthritis

[Display omitted] Osteoarthritis (OA) is a degenerative disease that leads to joint pain and stiffness and is one of the leading causes of disability and pain worldwide. Autophagy is a highly conserved self-degradation process, and its abnormal function is closely related to human diseases, including OA. Abnormal autophagy regulates cell aging, matrix metalloproteinase metabolism, and reactive oxygen metabolism, which are key in the occurrence and development of OA. There is evidence that drugs directly or indirectly targeting autophagy significantly hinder the progress of OA. In addition, the occurrence and development of autophagy in OA are regulated by many factors, including epigenetic modification, exosomes, crucial autophagy molecules, and signaling pathway regulation. Autophagy, as a new therapeutic target for OA, has widely influenced the pathological mechanism of OA. However, determining how autophagy affects OA pathology and its use in the treatment and diagnosis of targets still need further research.