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Her argument is that as we age, two things happen: we tend to have fewer mitochondria the mitochondria we do have are more vulnerable to damage That damage contributes to inflammation and poor cellular performance
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In addition to the above-mentioned GPX4-mediated classical ferroptosis pathway, the mitochondrial transmembrane channel VDAC (voltage-dependent anion channel) and the tumor suppressor gene P53 can also mediate ferroptosis [90,91]
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