ArticleOpen life sciences2025
Low-pressure exposure influences the development of HAPE.
Article in Open life sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Eleutheroside E Attenuates Hypobaric Hypoxia-Induced High Altitude Pulmonary Edema by Regulating Ferritinophagy-Mediated Ferroptosis via Keap1-Nrf2 Regulatory Axis.Journal of inflammation research · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-altitude pulmonary edema (HAPE) is non-cardiogenic pulmonary edema that occurs in healthy individuals who are unable to acclimatize when they ascend above 2,500-3,000 m above sea level in a few days. The pathogenesis of HAPE is complex and it is difficult to explain it by a single mechanism. Currently recognized pathogenesis is related to altered pulmonary hemodynamics, increased pulmonary capillary permeability, inflammatory response, dysregulated sodium-water transport, and impaired alveolar fluid clearance, and it is caused by a combination of causes. A high-altitude environment is both hypobaric and hypoxic, and whether hypobaria contributes to the pathogenesis of HAPE is unknown. We established a model in which 30 Institute of Cancer Research Mice (ICR mice) were divided into normal control (C,
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