ArticleScience advances2022
SARS-CoV-2 disrupts respiratory vascular barriers by suppressing Claudin-5 expression.
Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 74 citations in OpenAlex.
- Targeting claudins in cancer.Nature reviews. Drug discovery · 2026Review
- Respiratory Organ-on-a-Chip for Disease Modeling: From Architecture to Functional Integration.Advanced healthcare materials · 2026Review
- Shear cytokine crosstalk is a determinant of SARS-CoV-2-induced endothelial pathophysiology and thrombosis in human vessel chips.Journal of thrombosis and haemostasis : JTH · 2026Article
- From Endothelial Barrier Dysfunction to Circulating Biomarker: Clinical Potential of Claudin-5 in Thoracic Aortic Aneurysm and Dissection.Journal of clinical medicine · 2026Article
- Pathogenic breaches: how viruses compromise blood-tissue barriers.Tissue barriers · 2026Review
- A non-spike nucleocapsid R204P mutation in SARS-CoV-2 Omicron XEC enhances inflammation and pathogenicity.Nature communications · 2025Article
- Isogenic induced-pluripotent-stem-cell-derived airway- and alveolus-on-chip models reveal specific innate immune responses.Nature biomedical engineering · 2025Article
- Organoid Models to Study Human Infectious Diseases.Cell proliferation · 2025Review
- Monoclonal antibodies against human TMPRSS2 prevent infection by any SARS-CoV-2 variant.iScience · 2025Article
- Claudin 5 Across the Vascular Landscape: From Blood-Tissue Barrier Regulation to Disease Mechanisms.Cells · 2025Review
- In vitro biomimetic models for respiratory diseases: progress in lung organoids and lung-on-a-chip.Stem cell research & therapy · 2025Review
- Claudin-11 plays a pivotal role in the clathrin-mediated endocytosis of influenza A virus.Science China. Life sciences · 2025Article
- Advances in human organs-on-chips and applications for drug screening and personalized medicine.Fundamental research · 2025Review
- miR-27a-5p, miR-21-5p, miR-1246 and miR-4508: a candidate microRNA signature in the protection and regulation of viral infection in mild COVID-19.Molecular medicine (Cambridge, Mass.) · 2025Article
- Comparative temporal transcriptome analyses of SARS-CoV-2 delta and omicron variants ex-vivo infection in cat lung explant culture.Frontiers in cellular and infection microbiology · 2025Article
- Cholesterol and Cholesterol-Lowering Medications in COVID-19-An Unresolved Matter.International journal of molecular sciences · 2024Review
- Preeclampsia in the Context of COVID-19: Mechanisms, Pathophysiology, and Clinical Outcomes.American journal of reproductive immunology (New York, N.Y. : 1989) · 2024Review
- Sex differences in airway disease: estrogen and airway surface liquid dynamics.Biology of sex differences · 2024Review
- Virological characteristics of a SARS-CoV-2-related bat coronavirus, BANAL-20-236.EBioMedicine · 2024Article
- Endothelial ROBO4 suppresses PTGS2/COX-2 expression and inflammatory diseases.Communications biology · 2024Article
Corrections and comments
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Authors and funding
32 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the initial process of coronavirus disease 2019 (COVID-19), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infects respiratory epithelial cells and then transfers to other organs the blood vessels. It is believed that SARS-CoV-2 can pass the vascular wall by altering the endothelial barrier using an unknown mechanism. In this study, we investigated the effect of SARS-CoV-2 on the endothelial barrier using an airway-on-a-chip that mimics respiratory organs and found that SARS-CoV-2 produced from infected epithelial cells disrupts the barrier by decreasing Claudin-5 (CLDN5), a tight junction protein, and disrupting vascular endothelial cadherin-mediated adherens junctions. Consistently, the gene and protein expression levels of CLDN5 in the lungs of a patient with COVID-19 were decreased. CLDN5 overexpression or Fluvastatin treatment rescued the SARS-CoV-2-induced respiratory endothelial barrier disruption. We concluded that the down-regulation of CLDN5 expression is a pivotal mechanism for SARS-CoV-2-induced endothelial barrier disruption in respiratory organs and that inducing CLDN5 expression is a therapeutic strategy against COVID-19.
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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.