Mechanism: Aging mammals show iron accumulation due to impaired ferritin expression, ferroportin activity, and hepcidin regulation, leading to oxidative damage and ferroptosis. Readout: Readout: Long-lived species maintain iron homeostasis, resulting in lower iron load, reduced oxidative stress, and significantly extended lifespans.
Iron accumulation drives oxidative damage and ferroptosis in aging mammalian tissues. Long-lived species maintain iron homeostasis over centuries. The mechanism may be enhanced ferritin expression, ferroportin activity, and hepcidin regulation that mammals gradually lose.
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