The dysregulated autophagy in osteoarthritis: Revisiting molecular profile

The risk factors of osteoarthritis (OA) are different and obesity, lifestyle, inflammation, cell death mechanisms and diabetes mellitus are among them. The changes in the biological mechanisms are considered as main regulators of OA pathogenesis. The dysregulation of autophagy is observed in different human diseases. During the pathogenesis of OA, the autophagy levels (induction or inhibition) change. The supportive and pro-survival function of autophagy can retard the progression of OA. The protective autophagy prevents the cartilage degeneration. Moreover, autophagy demonstrates interactions with cell death mechanisms and through inhibition of apoptosis and necroptosis, it improves OA. The non-coding RNA molecules can regulate autophagy and through direct and indirect control of autophagy, they dually delay/increase OA pathogenesis. The mitochondrial integrity can be regulated by autophagy to alleviate OA. Furthermore, therapeutic compounds, especially phytochemicals, stimulate protective autophagy in chondrocytes to prevent cell death. The protective autophagy has ability of reducing inflammation and oxidative damage, as two key players in the pathogenesis of OA.