The interplay between autophagy and programmed cell death in osteoarthritis: insights into mechanisms and therapeutic targets.

Osteoarthritis is a common degenerative joint disorder characterized by cartilage damage causing pain and movement impairment. Its progression involves inflammatory responses, metabolic abnormalities, and cell death pathways including autophagy. This review elucidates the regulatory mechanisms of autophagy in programmed cell death and its impact on osteoarthritis. Studies demonstrate that autophagy can regulate apoptosis, necroptosis and other death pathways through specific components, distinguishing ''autophagy-mediated cell death'' from the direct elimination mechanism of ''autophagy-dependent cell death''. In osteoarthritis, autophagy participates in cartilage degeneration and joint inflammation by modulating inflammatory factors and stress responses. Understanding the dual regulatory mechanisms of autophagy provides theoretical foundations for developing targeted therapeutic strategies. This article systematically compares pathway characteristics of different autophagy-related cell death types, proposing that precise regulation of autophagy-mediated death processes may emerge as a novel approach to protect cartilage and delay disease progression. These research advances offer crucial theoretical support for precision medicine in osteoarthritis management.