ReviewAnnals of translational medicine2018
New insights into the mechanisms of pulmonary edema in acute lung injury.
Review in Annals of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04369820 (C5a Receptor Expression in Circulating Myeloid Cells in ARDS Secondary to COVID-19), which is not on this map. Cited by 116 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.
The trial behind it
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.
C5a Receptor Expression in Circulating Myeloid Cells in ARDS Secondary to COVID-19
Who cites it
116 citing papers in PubMed, 236 citations in OpenAlex.
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- Rosuvastatin Attenuates Pulmonary Damage in Rats with Cecal Ligation and Puncture-Induced Sepsis.Journal of clinical medicine · 2026Article
- A Fully Biological Gas-Exchange Membrane toward a Biofabricated, Booster Lung.ACS biomaterials science & engineering · 2026Article
- Cardiac Mitochondrial Dysfunction Following Bleomycin-Induced Acute Lung Injury in Rats.bioRxiv : the preprint server for biology · 2026Article
- Measuring and managing pulmonary edema in ARDS: a narrative review.Critical care (London, England) · 2026Review
- Alveolar-Basal Intermediates Drive Pulmonary Fibrosis via Coordination of a Pro-Fibrotic Signaling Niche in Silicosis.bioRxiv : the preprint server for biology · 2026Article
- Role of ITIH4 in Modulating YAP/TAZ-Mediated Apoptosis of Type II Alveolar Epithelium during Acute Respiratory Distress Syndrome.Pharmaceutical research · 2026Article
- LIMCH1-enriched extracellular vesicles promote vascular permeability in early-onset preeclampsia.Science advances · 2026Article
- Scutellarein fromPharmaceuticals (Basel, Switzerland) · 2026Article
- The Role and Mechanism of HIF-1α in Regulating A549 Alveolar Epithelial Cell Function Under Hypoxic Conditions.Canadian respiratory journal · 2026Article
- Liposomes as carriers for garlic oil delivery to increase anti-inflammatory and antioxidant activities in mice with ALI.Experimental biology and medicine (Maywood, N.J.) · 2026Article
- Leptospirosis-associated pulmonary hemorrhagic syndrome: immune mechanisms, clinical manifestations, and experimental models.Revista do Instituto de Medicina Tropical de Sao Paulo · 2026Review
- Elevated hydrostatic pressure destabilizes VE-cadherin junctions in a time and shear stress dependent manner: An endothelium-on-chip study.APL bioengineering · 2025Article
- Age Matters: Key Contributors to Interferon Toxicity in Infants During Influenza Virus Infection.Viruses · 2025Review
- Diosgenin ameliorates silica-induced tuberculosis in rats.Animal models and experimental medicine · 2025Article
- The lectin-like domain of TNF reduces pneumonia-induced injury in the perfused human lung.JCI insight · 2025Article
- Chitosan Nanoparticle-EncapsulatedInternational journal of molecular sciences · 2025Article
- Curcumin-loaded nanoemulsion for acute lung injury treatmentADMET & DMPK · 2025Article
56 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Appearance of alveolar protein-rich edema is an early event in the development of acute respiratory distress syndrome (ARDS). Alveolar edema in ARDS results from a significant increase in the permeability of the alveolar epithelial barrier, and represents one of the main factors that contribute to the hypoxemia in these patients. Damage of the alveolar epithelium is considered a major mechanism responsible for the increased pulmonary permeability, which results in edema fluid containing high concentrations of extravasated macromolecules in the alveoli. The breakdown of the alveolar-epithelial barrier is a consequence of multiple factors that include dysregulated inflammation, intense leukocyte infiltration, activation of pro-coagulant processes, cell death and mechanical stretch. The disruption of tight junction (TJ) complexes at the lateral contact of epithelial cells, the loss of contact between epithelial cells and extracellular matrix (ECM), and relevant changes in the communication between epithelial and immune cells, are deleterious alterations that mediate the disruption of the alveolar epithelial barrier and thereby the formation of lung edema in 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.