ArticleAmerican journal of respiratory cell and molecular biology2025
Endothelial ENaC-α Restrains Oxidative Stress in Lung Capillaries in Murine Pneumococcal Pneumonia-associated Acute Lung Injury.
Article in American journal of respiratory cell and molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Histone acetylation-regulated FBXO11-dependent degradation of BLIMP-1 promotes lung injury.Translational pediatrics · 2026Article
- Early-life lung injury and the developing brain: a lung-brain axis perspective on neurodevelopmental disorders.Journal of neuroinflammation · 2026Review
- Nox1-Derived ROS Amplifies Calcium Entry and Enhances Pneumolysin-Induced Lung Endothelial Barrier Dysfunction in Hyperglycemia.Antioxidants (Basel, Switzerland) · 2026Article
- Association and incremental predictive value of preoperative AISI and CALLY for postoperative pulmonary complications after McKeown esophagectomy following neoadjuvant chemoimmunotherapy.Frontiers in immunology · 2026Article
- Pharmacologic depletion of border-associated macrophages worsens disease in a mouse model of meningitis.Acta neuropathologica communications · 2025Article
- The lectin-like domain of TNF reduces pneumonia-induced injury in the perfused human lung.JCI insight · 2025Article
- Can ENaC "TIP" the Scales to Reduce Endothelial Reactive Oxygen Species and Vascular Leak during Pneumococcal Lung Injury?American journal of respiratory cell and molecular biology · 2025Article
- Endothelial ENaC as a repressor of oxidative stress and a guardian of lung capillary barrier function in bacterial and viral pneumonia.Frontiers in physiology · 2025Review
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27 authors.
Funding
Abstract
Infection of lung endothelial cells with pneumococci activates the superoxide-generating enzyme NOX2 (nicotinamide adenine dinucleotide phosphate hydrogen [NADPH] oxidase 2), involving the pneumococcal virulence factor PLY (pneumolysin). Excessive NOX2 activity disturbs capillary barriers, but its global inhibition can impair bactericidal phagocyte activity during pneumococcal pneumonia. Depletion of the α subunit of ENaC (epithelial sodium channel) in pulmonary endothelial cells increases expression and PMA-induced activity of NOX2. Direct ENaC activation by TIP peptide improves capillary barrier function-measured by electrical cell substrate impedance sensing in endothelial monolayers and by Evans blue dye incorporation in mouse lungs-after infection with pneumococci. PLY-induced hyperpermeability in human lung microvascular endothelial cell monolayers is abrogated by both NOX2 inhibitor gp91dstat and TIP peptide. Endothelial NOX2 expression is assessed by increased surface membrane presence of phosphorylated p47
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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 Socratic graph.