ArticleScientific reports2025
Integrative proteomics and metabolomics reveal important pathways and potential biomarkers in high-altitude pulmonary hypertension.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Artificial Intelligence and Multi-Omics Approaches in the Precision Management of Pulmonary Hypertension: From Early Diagnosis to Therapeutic Stratification.International journal of molecular sciences · 2026Review
- Proteomic study of high-altitude pulmonary hypertension in the Xinjiang Pamir highlanders.BMC pulmonary medicine · 2026Article
- Roles of Lipid Metabolism in Pulmonary Hypertension: Friend or Foe?Biomolecules · 2025Review
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Authors and funding
9 authors.
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Abstract
High-altitude pulmonary hypertension (HAPH) is a severe condition affecting highland residents, yet its molecular mechanisms remain incompletely understood. This study aimed to investigate the pathogenesis of HAPH through integrated metabolomic and proteomic analyses. We performed untargeted metabolomics and proteomics analyses on plasma samples from HAPH patients (n=30) and matched healthy controls (n=30). Differential expression analysis, pathway enrichment, and integrated multi-omics analysis were conducted. Key findings were validated using targeted proteomics (PRM). We identified 26 differentially expressed metabolites (12 upregulated, 14 downregulated) and 35 differentially expressed proteins (5 upregulated, 30 downregulated) in HAPH patients. Integrated pathway analysis revealed significant alterations in glycerophospholipid metabolism (PC(20:4/8Z,11Z), FC = 2.804, P.adjust = 0.047), immune response (IGLL1, FC = -1.557, P.adjust = 0.003), cytoskeletal organization (MYH10, FC = 7.574, P.adjust =0.189), and oxidative stress response pathways. PRM validation confirmed the differential expression of five key proteins: ACTG1, VNN1, CKB (upregulated), and APOF and CST3 (downregulated). Our integrated multi-omics analysis reveals a complex molecular network underlying HAPH pathogenesis, characterized by coordinated changes in lipid metabolism, immune function, and cellular structure. These findings provide new insights into HAPH mechanisms and identify potential therapeutic targets for intervention.
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