ReviewInternational journal of general medicine2026
Targeting Ferroptosis for Cerebral Neuroprotection in Ischemic Stroke: Pathophysiological Insights.
Review in International journal of general medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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5 authors.
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Abstract
Acute ischemic stroke, a leading cause of neurological disability, stemed from cerebral hypoperfusion-induced ischemia/reperfusion (I/R) injury. Ferroptosis, an iron-dependent, lipid peroxidation-driven cell death, has emerged as a key pathological driver. Unlike apoptosis, ferroptosis involves glutathione peroxidase 4 (GPX4) inactivation, iron dysregulation, and lethal lipid peroxides. Its preclinical inhibition reduced neuronal loss, demonstrating therapeutic promise. Ischemic injury activated accidental/regulated cell death pathways, with ferroptosis, apoptosis, and pyroptosis dynamically regulated by ischemia duration/severity. Convergent mechanisms included hypoxia-induced mitochondrial dysfunction, iron/lipid peroxidation disrupting blood-brain barrier integrity, glutamate-ferroptosis oxidative crosstalk, and Ca
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