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Corroborative animal research showed that both dietary and environmental exposure to acrolein exacerbated myocardial ischemic injury and atherosclerosis in mouse models, presumably by interacting with endogenous unsaturated aldehydes generated during ongoing oxidative stress [55], [58], [63], [71]

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However, PD-1 and PD-L1 transcripts are expressed only at very low levels in these datasets, limiting direct inference of checkpoint-mediated ferroptosis regulation in AD

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