Epigenetic modification and exosome effects on autophagy in osteoarthritis

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.

Automated summary

Osteoarthritis is a leading cause of disability and pain worldwide, and abnormal autophagy has been closely associated with this degenerative disease. Drugs targeting autophagy have shown significant potential in hindering the progression of osteoarthritis. The occurrence and development of autophagy in osteoarthritis are regulated by various factors, and it has greatly influenced the pathological mechanism of the disease. However, further research is needed to determine how autophagy affects the pathology of osteoarthritis and its application in treatment and diagnosis.