ArticleActa physiologica (Oxford, England)2020
Deregulated hypoxic response in myeloid cells: A model for high-altitude pulmonary oedema (HAPE).
Article in Acta physiologica (Oxford, England), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 20 citations in OpenAlex.
- 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
- Research progress on high-altitude hypoxia pulmonary injury: pathogenesis and Chinese herbal medicine for prevention and treatment.Frontiers in pharmacology · 2026Review
- Enhancing Quercetin's Potential: A Nanoliposome Delivery System for High Altitude Pulmonary Edema.Drug design, development and therapy · 2025Article
- Effect of furosemide in the treatment of high-altitude pulmonary edema.BMC pulmonary medicine · 2024Article
- Research Progress on the Mechanism of Right Heart-Related Pulmonary Edema.Evidence-based complementary and alternative medicine : eCAM · 2022Review
- Deregulated hypoxic response in myeloid cells: A model for high-altitude pulmonary oedema (HAPE).Acta physiologica (Oxford, England) · 2020Article
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5 authors at 3 institutions in 3 countries.
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Abstract
aimHigh-altitude pulmonary oedema (HAPE) is a non-cardiogenic pulmonary oedema that can occur during rapid ascent to a high-altitude environment. Classically, HAPE has been described as a condition resulting from a combination of pulmonary vasoconstriction and hypertension. Inflammation has been described as important in HAPE, although as a side effect of pulmonary oedema rather than as a causative factor. In this study, we aim to understand the role of hypoxic response in myeloid cells and its involvement in pathogenesis of HAPE.
methodsWe have generated a conditional deletion in mice of the von Hippel-Lindau factor (VHL) in myeloid cells to determine the effect of a deregulated hypoxic response in pulmonary oedema.
resultsThe deletion of VHL in pulmonary myeloid cells gave rise to pulmonary oedema, increased pulmonary vascular permeability and reduced performance during exertion. These changes were accompanied by reduced stroke volume in the left ventricle.
conclusionIn this model, we show that a deregulated myeloid cell hypoxic response can trigger some of the most important symptoms of HAPE, and thus mice with a deletion of VHL in the myeloid lineage can function as a model of HAPE.
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