ArticleAmerican journal of physiology. Lung cellular and molecular physiology2021
Molecular mechanisms of Na,K-ATPase dysregulation driving alveolar epithelial barrier failure in severe COVID-19.
Article in American journal of physiology. Lung cellular and molecular physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Heart failure during the COVID-19 pandemic: clinical, diagnostic, management, and organizational dilemmas.ESC heart failure · 2022Pooled it
- The impact of perfusate filtration or exchange on lung function during ex vivo lung perfusion (EVLP): a systematic review.Journal of thoracic disease · 2026Review
- Respiratory epithelial cells as central mediators of immune crosstalk in SARS-CoV-2 infection.Frontiers in immunology · 2026Review
- Minimalistic transcriptomic signatures permit accurate early prediction of COVID-19 mortality.JCI insight · 2025Article
- The role of Na,K‑ATPase in lung diseases (Review).Molecular medicine reports · 2025Review
- Sensing molecular carbon dioxide: a translational focus for respiratory disease.Physiological reviews · 2025Review
- SARS-CoV-2 S, M, and E Structural Glycoproteins Differentially Modulate Endoplasmic Reticulum Stress Responses.International journal of molecular sciences · 2025Article
- NaInternational journal of molecular sciences · 2024Review
- Blood metal analysis of plasmas from donors with and without SARS-CoV-2 using laser-induced breakdown spectroscopy and logistic regression.Biomedical optics express · 2024Article
- Sodium Glucose Transporter-2 Inhibitors (SGLT2Is)-TLRs Axis Modulates Diabetes.Cell biochemistry and biophysics · 2023Review
- Fibrinolytic system and COVID-19: From an innovative view of epithelial ion transport.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Review
- Determining human-coronavirus protein-protein interaction using machine intelligence.Medicine in novel technology and devices · 2023Article
- Roles of the ACE/Ang II/AT1R pathway, cytokine release, and alteration of tight junctions in COVID-19 pathogenesis.Tissue barriers · 2023Article
- Clathrin-Mediated Albumin Clearance in Alveolar Epithelial Cells of Murine Precision-Cut Lung Slices.International journal of molecular sciences · 2023Article
- Direct endothelial ENaC activation mitigates vasculopathy induced by SARS-CoV2 spike protein.Frontiers in immunology · 2023Article
- Understanding COVID-19 susceptibility and presentation based on its underlying physiology.Physiological reviews · 2022Article
- Human placenta-derived amniotic epithelial cells as a new therapeutic hope for COVID-19-associated acute respiratory distress syndrome (ARDS) and systemic inflammation.Stem cell research & therapy · 2022Review
- Review
- Extranuclear effects of thyroid hormones and analogs during development: An old mechanism with emerging roles.Frontiers in endocrinology · 2022Review
- Displacement of Native FXYD Protein From NaFrontiers in oncology · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
A significant number of patients with coronavirus disease 2019 (COVID-19) develop acute respiratory distress syndrome (ARDS) that is associated with a poor outcome. The molecular mechanisms driving failure of the alveolar barrier upon severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection remain incompletely understood. The Na,K-ATPase is an adhesion molecule and a plasma membrane transporter that is critically required for proper alveolar epithelial function by both promoting barrier integrity and resolution of excess alveolar fluid, thus enabling appropriate gas exchange. However, numerous SARS-CoV-2-mediated and COVID-19-related signals directly or indirectly impair the function of the Na,K-ATPase, thereby potentially contributing to disease progression. In this Perspective, we highlight some of the putative mechanisms of SARS-CoV-2-driven dysfunction of the Na,K-ATPase, focusing on expression, maturation, and trafficking of the transporter. A therapeutic mean to selectively inhibit the maladaptive signals that impair the Na,K-ATPase upon SARS-CoV-2 infection might be effective in reestablishing the alveolar epithelial barrier and promoting alveolar fluid clearance and thus advantageous in patients with COVID-19-associated ARDS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.