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Ischemic stroke begins with a sudden interruption of blood flow to the brain, but the damage does not stop when blood flow is restored. The initial ischemic insult triggers a series of secondary events, including inflammation, oxidative stress, cell death, and disrupted genomic regulation. These can continue to damage the brain well beyond the initial vascular event. Mapping the molecular pathways that link ischemic stress to this secondary injury remains one of the persistent challenges in stroke research.
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Bazaz et al. (2026) studied this question.
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