ArticleCNS neuroscience & therapeutics2026
High-Altitude Hypoxia Activates JNK-p53 Signaling: Linking Hippocampal Energy Crisis to Cognitive Impairment.
Article in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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7 authors.
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Abstract
backgroundChronic high-altitude hypoxia impairs hippocampal memory, yet population-level dose-response relationships and the molecular mechanisms linking hypoxic stress to energy metabolic collapse remain poorly defined.
methodsWe conducted a cross-sectional study of 2819 residents (living at altitudes between 3000 and 5000 m). In parallel, we established a rat model of sustained hypobaric hypoxia (6000 m, 1-28 days) and applied pharmacological intervention using the JNK inhibitor JNK-IN-8. Metabolomic profiling, transmission electron microscopy, and molecular analyses were performed to assess metabolic reprogramming, mitochondrial ultrastructure, and signaling pathways.
resultsResidents at > 4000 m exhibited 91% higher memory impairment risk. Chronic hypoxia activated JNK-p53-Bim signaling, driving mitophagy-to-apoptosis transition, mitochondrial cristae disruption, and 73% ATP depletion by Day 28. JNK-IN-8 partially restored ATP and suppressed p53. HIF-2α/PHD2 colocalization indicated parallel adaptive signaling.
conclusionsChronic hypoxia induces memory impairment via JNK-mediated mitochondrial dysfunction. JNK inhibition offers therapeutic potential, while concurrent HIF-2α/PHD2 activation suggests a complex balance between hypoxic injury and adaptation.
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