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High-dose ferric ammonium citrate (FeAC) triggers MM cell death with concurrent elevation of MDA - a lipid peroxidation byproduct and hallmark of ferroptosis, establishing iron metabolism as a critical modulator in MM pathophysiology (Nemeth and Ganz, 2023), MM patients exhibit paradoxical hepcidin downregulation or functional impairment during iron overload, creating a self-reinforcing cycle of iron accumulation that exacerbates disease progression (Maes et al., 2010
[1] [2] These medications work by mimicking the action of natural GLP-1, binding to GLP-1 receptors throughout the body
Through its effects on metal availability, redox metabolism, and oxidative signaling, GSH can promote conditions that favor regulated cell death and may therefore be exploited for precision cancer therapy
Zanco Journal of Medical Sciences (ZJMS) , 22 (2), 227237.
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