Polyamines buffer labile iron to suppress ferroptosis
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Polyamines act as endogenous buffers of redox-active iron, with depletion increasing labile iron and promoting ferroptosis in mammalian cells.
- Why it matters: Understanding how cells regulate iron and prevent ferroptosis is crucial for developing therapies for diseases linked to oxidative stress and iron imbalance.
- What they did: Using genome-wide CRISPR screens and a novel fluorescent reporter, the study examined the relationship between polyamine levels and iron homeostasis in living cells, focusing on ferroptosis suppression.
- The result: Findings demonstrate that polyamines inversely regulate redox-active iron, revealing their role as key modulators of iron balance and ferroptosis, with potential implications for disease treatment.