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In addition to the primary triggers of ferroptosis in OA (iron overload, mechanical overload, and inflammatory responses) discussed above, several other factors may further enhance ferroptosis in this context: (i) Elevated levels of ROS : These arise from mechanical stress, inflammatory responses and mitochondrial dysfunction, contribute significantly to ferroptosis by predisposing chondrocytes to oxidative damage, as these cells are particularly vulnerable to such stressors [126, 127, 128]

Mitochondria autophagy is induced after hypoxic/ischemic stress in a Drp1 dependent manner: the role of inhibition of Drp1 in ischemic brain damage

Preclinical studies demonstrate that inhibition of WNT decreases renal WNT3a levels, improves autophagic flux, and attenuates glomerulosclerosis and interstitial fibrosis, which are closely correlated with reduced CD68+ macrophage infiltration and IL-17 secretion (159)

McQueen T, Konopleva M, Andreeff M
