Regulation of alveolar epithelial function by hypoxia

Zhou, G.; Dada, L. A.; Sznajder, J. I.

doi:10.1183/09031936.00155507

Cited by 57Ion Transport and Channel RegulationRespiratory Support and MechanismsHigh Altitude and Hypoxia

Regulation of alveolar epithelial function by hypoxia

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Zhou, G., Dada, L. A., Sznajder, J. I.·2008·European Respiratory Journal

DOI 10.1183/09031936.00155507

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Abstract

Patients with acute respiratory distress syndrome and high-altitude pulmonary oedema build up excess lung fluid, which leads to alveolar hypoxia. In patients with acute respiratory distress syndrome and hypoxia, there is a decrease in oedema fluid clearance, due in part to the downregulation of plasma membrane sodium-potassium adenosine triphosphatase (Na,K-ATPase). In alveolar epithelial cells, acute hypoxia promotes Na,K-ATPase endocytosis from the plasma membrane to intracellular compartments, resulting in inhibition of Na,K-ATPase activity. Exposure to prolonged hypoxia leads to degradation of plasma membrane Na,K-ATPase. The downregulation of plasma membrane Na,K-ATPase reduces adenosine triphosphate demand, as part of a survival mechanism of cellular adaptation to hypoxia. Hypoxia has also been shown to disassemble and degrade the keratin intermediate filament network, a fundamental component of the cell cytoskeleton, affecting epithelial barrier function. Accordingly, better understanding of the mechanisms regulating cellular adaptation to hypoxia may lead to the development of novel therapeutic strategies for acute respiratory distress syndrome and high-altitude pulmonary oedema patients.

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Hypoxic downregulation of Na/K-ATPase activity has important implications for airway fluid absorption during hypoxia.
“Thus, hypoxic downregulation of Na/K-ATPase activity has important implications for airway fluid absorption during hypoxia 22.”
From Mitochondrial reactive oxygen species regulate cellular signaling and dictate biological outcomes (2010) · cites this paper as [22]

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Authors: Zhou, G., Dada, L. A., & Sznajder, J. I.
Affiliations: Northwestern University (US)
ORCID: Zhou, G.
Dada, L. A.
Sznajder, J. I.
Venue: European Respiratory Journal
Publisher: European Respiratory Society (ERS)
Published: 2008-04-30
Volume: 31
Issue: 5
Pages: 1107-1113
ISSN: 0903-1936 (ISSN-L)
1399-3003
DOI: 10.1183/09031936.00155507
OpenAlex: W2101358905
Cited by: 57
References: 91
Citations by year: 2026: 3 · 2025: 2 · 2024: 3 · 2023: 3 · 2022: 2 · 2021: 2 · 2019: 1 · 2018: 2 · 2017: 6 · 2016: 4 · 2015: 1 · 2014: 4 · 2013: 5 · 2012: 5
FWCI: 0.36
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: European Respiratory Journal (publishedVersion)
PubMed (publishedVersion)
Funders: Northwestern University
National Institutes of Health (HL-071643)
Feinberg School of Medicine
National Heart, Lung, and Blood Institute (HL 48129, P01HL071643, HL 071643)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Respiratory Support and Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › High Altitude and Hypoxia
Keywords: alveolar epithelial cells, hypoxia, acute respiratory distress syndrome, high altitude pulmonary edema, alveolar hypoxia, Na+/K+-ATPase, epithelial barrier function, keratin intermediate filaments, cytoskeleton, alveolar edema
MeSH terms: Sodium-Potassium-Exchanging ATPase, Hypoxia, Cell Membrane, Epithelial Cells, Humans, Intermediate Filaments, Pulmonary Alveoli, Pulmonary Edema, Respiratory Distress Syndrome

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Regulation of alveolar epithelial function by hypoxia

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