Programmed cell death in osteoarthritis

Osteoarthritis (OA) is a prevalent degenerative joint disease with complex and multifactorial etiology, primarily affecting elderly populations. Factors such as mechanical stress and aging contribute to cartilage degeneration and joint damage. OA manifests through extracellular matrix (ECM) degradation in chondrocytes, decreased chondrocyte viability, and is associated with significant incidence and disability. Recent research indicates that multiple patterns of programmed cell death (PCD), including apoptosis, pyroptosis, necroptosis, autophagy, ferroptosis, cuproptosis, and PANoptosis, regulate the survival and death of chondrocytes through intricate molecular networks, thereby contributing to the onset and progression of OA.This review elucidates the molecular underpinnings of these seven forms of PCD and emphasizes their significance in OA pathology, with a view to providing new perspectives for in-depth research into the pathogenesis of OA and the development of targeted drugs.