Inhibition of apoptosis leads to defective follicular atresia and accumulation of immature follicles; pyroptosis and necroptosis amplify inflammatory cascades, promoting ovarian fibrosis and aggravating insulin resistance; ferroptosis induces lipid peroxidation–mediated granulosa cell injury, thereby reducing follicle-stimulating hormone (FSH) sensitivity; dysregulated autophagy exacerbates ferroptosis through ferritinophagy and degradation of GPX4. This evidence concerns the gene GPX4 and Insulin resistance.