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Kroner et al (49) demonstrated that elevated iron levels in microglia promote phagocytosis and drive a harmful M1 phenotype, which triggers the release of pro-inflammatory factors such as TNF-, IL-1, IL-6 and nitric oxide (NO), causing neuronal damage

Consequently, the accumulation of AP sites is mutagenic and will yield cell death

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Quantitative proteomic analyses reveal that GPX4 downregulation during myocardial infarction contributes to ferroptosis in cardiomyocytes

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