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Dysregulated iron homeostasis amplifies ferroptotic susceptibility through Fenton chemistry-driven lipid peroxidation and polyamine synthesis via the ODC1-MYC axis, a metabolic and oxidative cascade prominently observed in the inflamed synovium of rheumatoid arthritis ( Inducing ferroptosis in specific cell populations using agents like Imidazole ketone erastin (IKE) can suppress synovial fibroblast proliferation and inflammation (104)

This selective receptor interaction enables reproducible activation of intracellular signaling pathways associated with growth hormone synthesis and secretion (10)