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Researchers have also observed that glutathione regulates protein function through reversible S-glutathionylation of cysteine residues, modulating the activity of signaling proteins, transcription factors, and metabolic enzymes in response to oxidative conditions

Recent research has shown that DOX-induced ferroptosis in cardiomyocytes is reliant on GPX4, specifically GPX4 in mitochondria

486 This dysfunction is driven by ROS, oxidative lipids, endoplasmic reticulum (ER) stress, and genetic predispositions, all of which are worsened by caloric excess

This process facilitates the clearance of damaged mitochondria and misfolded proteins by chondrocytes, thereby maintaining intracellular homeostasis and delaying cellular senescence and degenerative changes