ArticleFrontiers in physiology2022
Soluble P-Selectin and von Willebrand Factor Rise in Healthy Volunteers Following Non-exertional Ascent to High Altitude.
Article in Frontiers in physiology, 2022. 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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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.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Hypoxia suppresses platelet activity through GPVI down-regulation but paradoxically enhances arterial thrombosis via elevated vWF.Cardiovascular research · 2026Article
- Human umbilical cord mesenchymal stem cells reduce platelet α-granule release in ratsWorld journal of stem cells · 2025Article
- A single-cell atlas of West African lungfish respiratory system reveals evolutionary adaptations to terrestrialization.Nature communications · 2023Article
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Authors and funding
6 authors at 3 institutions in 1 country.
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Abstract
Reduced oxygen tensions experienced at high altitudes are thought to predispose to thrombosis, yet there are few studies linking hypoxia, platelet activation, and thrombosis. Reports of platelet phenotypes in hypoxia are inconsistent, perhaps due to differing degrees of hypoxia experienced and the duration of exposure. This study aimed to investigate the relationship between soluble P-selectin, a marker of platelet activation, and von Willebrand factor (vWF) on exposure to hypoxia. We measured plasma concentrations of P-selectin and vWF in sixteen healthy volunteers before, during and after the APEX 2 expedition. APEX 2 consisted of a non-exertional ascent to 5,200 m, followed by 7 consecutive days at high altitude. We showed that high altitude significantly increased mean plasma P-selectin and vWF compared to pre-expedition levels. Both plasma marker levels returned to baseline post-expedition. We found a strong positive correlation between vWF and P-selectin, but no association between P-selectin and platelet count. Our results are consistent with previous work showing evidence of platelet activation at high altitude and demonstrate that the rise in P-selectin is not simply due to an increase in platelet count. As vWF and P-selectin could be derived from either platelets or endothelial cells, further work assessing more specific markers of endothelial activation is proposed to provide insight into the source of these potential pro-thrombotic biomarkers at altitude.
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