BackgroundHigh-altitude cerebral edema (HACE) is a life-threatening condition following rapid ascent to high altitude, with acute mountain sickness (AMS) as a key precursor. Increasing evidence implicates inflammation in its pathogenesis, yet the molecular regulatory networks remain unclear.MethodsWe integrated bulk RNA-seq (GSE75665), non-coding RNA-seq (GSE90500), and single-cell RNA-seq datasets to explore inflammation-related mechanisms in AMS.
Differentially expressed genes (DEGs) were identified and analyzed using Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA). Protein-protein interaction, miRNA-mRNA, transcription factor, and drug-gene networks were constructed.
Single-cell and deconvolution analyses determined cell-type-specific expression and immune composition. A hypobaric hypoxia-induced HACE mouse model was established for experimental validation to assess heparin-binding EGF-like growth factor (HBEGF) expression and associated neuroinflammatory and pathological changes.ResultsWe identified 323 DEGs, including five 5 inflammation-related genes, all downregulated in AMS and enriched in epithelial cell growth, migration, and the ErbB signaling pathway.
hsa-miR-375 was predicted to regulate multiple key genes, and drug gene analysis highlighted HBEGF as a potential therapeutic target.
Frontiers in Immunology published a clinical update in Infectious Disease on 22 May 2026.
The item focuses on Integrative multi-omics analysis reveals inflammation-related molecular networks in acute mountain sickness.
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