ArticleAging2020
The IL1β-HER2-CLDN18/CLDN4 axis mediates lung barrier damage in ARDS.
Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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
16 citing papers in PubMed.
- Air pollution-induced airway epithelial barrier dysfunction in COPD: a narrative review of mechanisms and therapeutic implications.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Targeting Claudin18.2 for cancer theranostics: From molecular imaging to precision therapy.iScience · 2025Review
- Review
- The Synthetic LXR Agonist GW3965 Attenuates Phosgene-Induced Acute Lung Injury Through the Modulation of PI3K/Akt and NF-κB Signalling Pathways.Basic & clinical pharmacology & toxicology · 2025Article
- Article
- Silicosis: from pathogenesis to therapeutics.Frontiers in pharmacology · 2025Review
- Disruption of pulmonary microvascular endothelial barrier by dysregulated claudin-8 and claudin-4: uncovered mechanisms in porcine reproductive and respiratory syndrome virus infection.Cellular and molecular life sciences : CMLS · 2024Article
- Zolbetuximab for Claudin18.2-positive gastric or gastroesophageal junction cancer.Therapeutic advances in medical oncology · 2024Review
- Anticancer pan-ErbB inhibitors reduce inflammation and tissue injury and exert broad-spectrum antiviral effects.The Journal of clinical investigation · 2023Article
- The Na/K-ATPase role as a signal transducer in lung inflammation.Frontiers in immunology · 2023Review
- Targeting CLDN18.2 in cancers of the gastrointestinal tract: New drugs and new indications.Frontiers in oncology · 2023Review
- Dexamethasone restores TNFα-induced epithelial barrier dysfunction in primary rat alveolar epithelial cells.PloS one · 2023Article
- Dysfunction of epithelial permeability barrier induced by HMGB1 in 2.5D cultures of human epithelial cells.Tissue barriers · 2022Review
- Role of air pollutants in airway epithelial barrier dysfunction in asthma and COPD.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Investigating the Intercellular Communication Network of Immune Cell in Acute Respiratory Distress Syndrome with Sepsis.Computational and mathematical methods in medicine · 2022Article
- IL-1β and the Intestinal Epithelial Tight Junction Barrier.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe high mortality rate associated with acute respiratory distress syndrome (ARDS) is a major challenge for intensive care units. In the present study, we applied bioinformatics and animal models to identify core genes and potential corresponding pathways in ARDS.
resultsUsing bioinformatics analysis, IL-1β was identified as the core gene of ARDS. Cell experiments showed that up-regulation of IL-1β downregulates claudin18 to promote lung barrier function damage by regulating the IL-1β-HER2/HER3 axis, further promoting the development of ARDS. This was validated in the animal models.
conclusionIL-1β promotes the development of ARDS by regulating the IL-1β-HER2/HER3 axis. These findings deepen the understanding of the pathological mechanisms of ARDS.
methodsTranscription data sets related to ARDS were subjected to differential expression gene analysis, functional enrichment analysis, and receiver operating characteristic curve analysis and, so as to identify core genes in ARDS. Cell experiments were used to further explore the effects of core genes on lung barrier function damage. Animal models were applied to validate the effects of core gene in mediating biological signal pathways 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.