ArticleApoptosis : an international journal on programmed cell death2024
TNF-α and RPLP0 drive the apoptosis of endothelial cells and increase susceptibility to high-altitude pulmonary edema.
Article in Apoptosis : an international journal on programmed cell death, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Driving pressure guided ventilation with lung ultrasound reduces pulmonary complications after epigastric surgery at high altitude.Scientific reports · 2026Trial
- Melatonin treatment alters cardiopulmonary structure, function, and acute hypoxic response in the newborn lamb.Pediatric research · 2026Article
- Plasma multi-omics profiling unravels molecular alterations and biomarker panels during recovery from severe coronavirus disease 2019: a pilot study.BMC infectious diseases · 2026Article
- Prophylactic Nebulized hUC-MSC-EVs Attenuate Hypobaric Hypoxia-Induced Lung Injury via Alveolar-Capillary Barrier Stabilization and TEK/Tie2 Preservation.Biomedicines · 2026Article
- Hypobaric hypoxia can lead to an increase in lung dendritic cells and promote T-cell immunosuppression, thereby preventing the excessive progression of high-altitude pulmonary edema.Frontiers in immunology · 2026Article
- Integrative blood profiling uncovers inflammatory network signatures in high-altitude pulmonary edema.Bioscience reports · 2025Article
- Citri Sarcodactylis Fructus Alleviates LPS-Induced Acute Lung Injury by Inhibiting Inflammation and Inflammasome Activation.Food science & nutrition · 2025Article
- Deciphering Oxidative Stress in Cardiovascular Disease Progression: A Blueprint for Mechanistic Understanding and Therapeutic Innovation.Antioxidants (Basel, Switzerland) · 2024Review
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12 authors.
Funding
Abstract
High-altitude pulmonary edema (HAPE) is a fatal threat for sojourners who ascend rapidly without sufficient acclimatization. Acclimatized sojourners and adapted natives are both insensitive to HAPE but have different physiological traits and molecular bases. In this study, based on GSE52209, the gene expression profiles of HAPE patients were compared with those of acclimatized sojourners and adapted natives, with the common and divergent differentially expressed genes (DEGs) and their hub genes identified, respectively. Bioinformatic methodologies for functional enrichment analysis, immune infiltration, diagnostic model construction, competing endogenous RNA (ceRNA) analysis and drug prediction were performed to detect potential biological functions and molecular mechanisms. Next, an array of in vivo experiments in a HAPE rat model and in vitro experiments in HUVECs were conducted to verify the results of the bioinformatic analysis. The enriched pathways of DEGs and immune landscapes for HAPE were significantly different between sojourners and natives, and the common DEGs were enriched mainly in the pathways of development and immunity. Nomograms revealed that the upregulation of TNF-α and downregulation of RPLP0 exhibited high diagnostic efficiency for HAPE in both sojourners and natives, which was further validated in the HAPE rat model. The addition of TNF-α and RPLP0 knockdown activated apoptosis signaling in endothelial cells (ECs) and enhanced endothelial permeability. In conclusion, TNF-α and RPLP0 are shared biomarkers and molecular bases for HAPE susceptibility during the acclimatization/adaptation/maladaptation processes in sojourners and natives, inspiring new ideas for predicting and treating HAPE.
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