Abstract
Osteoarthritis (OA) is a degenerative joint disease characterized by the breakdown of cartilage and the subsequent inflammation of joint tissues, leading to pain and reduced mobility. Despite advancements in symptomatic treatments, disease-modifying therapies for OA remain limited. This narrative review examines the dual role of autophagy in OA, emphasizing its protective functions during the early stages and its potential to contribute to cartilage degeneration in later stages. By delving into the molecular pathways that regulate autophagy, this review highlights its intricate interplay with oxidative stress and inflammation, key drivers of OA progression. Emerging therapeutic strategies aimed at modulating autophagy are explored, including pharmacological agents such as AMP kinase activators, and microRNA-based therapies. Preclinical studies reveal encouraging results, demonstrating that enhancing autophagy can reduce inflammation and decelerate cartilage degradation. However, the therapeutic benefits of autophagy modulation depend on precise, stage-specific approaches. Excessive or dysregulated autophagy in advanced OA may lead to chondrocyte apoptosis, exacerbating joint damage. This review underscores the promise of autophagy-based interventions in bridging the gap between experimental research and clinical application. By advancing our understanding of autophagy's role in OA, these findings pave the way for innovative and effective therapies. Nonetheless, further research is essential to optimize these strategies, address potential off-target effects, and develop safe, targeted treatments that improve outcomes for OA patients.