Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article 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.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9491726 | PMC |
| http://dx.doi.org/10.1126/sciadv.abo6783 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
WNT7A/B assemble a GPR124-RECK-LRP5/6 co-receptor complex to activate β-catenin signaling in brain endothelial cells.
J Biol Chem
September 2025
Institute of Anatomy and Cell Biology, University of Würzburg, Würzburg, Germany. Electronic address:
WNT7A and WNT7B, secreted by neural cells, are essential regulators of developmental brain angiogenesis and blood-brain barrier integrity. In brain endothelial cells, WNT7 proteins activate β-catenin signaling through the ligand-specific receptor complex GPR124-RECK and classical WNT receptors of the FZD and LRP families. Previous studies suggested that WNT7 isoforms assemble a GPR124-RECK-FZD-LRP5/6 multi-receptor complex for signaling.
View Article and Find Full Text PDFNickel exposure aggravates aortic dissection by exacerbating neutrophil recruitment and NETosis to compromise endothelial barrier.
J Hazard Mater
September 2025
State Key Laboratory of Reproductive Medicine and Offspring Health, School of Public Health, Nanjing Medical University, Nanjing, China; Jiangsu Environmental Health Risk Assessment Engineering Research Center, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, N
Nickel exposure elevates aortic dissection (AD) risk, yet its pathogenic mechanisms remain unclear. Here, we demonstrate that nickel accelerates AD progression, particularly in hypertensive individuals. Bioinformatics analysis of GEO datasets identified chemokine-mediated endothelial-neutrophil crosstalk as a key pathway.
View Article and Find Full Text PDFZwitterionic Sulfadiazine-Based Micelle Achieves Effective Drug Delivery to Glioblastoma by Overcoming Multiple Biological Barriers.
J Am Chem Soc
September 2025
College of Medical Engineering, Beijing Institute of Technology, 6 Jinfeng Road, Zhuhai, 519088, China.
Multiple biological barriers severely restrict the delivery efficiency of nanoparticles (NPs) to tumors. To overcome biological barriers, traditional NPs usually require a complex design, which increases the difficulty of clinical translation. Therefore, there appears to be a dilemma between the complex biological barriers and clinical requirement for a simple molecular structure of NPs.
View Article and Find Full Text PDFUnifying Vascular Injury and Neurodegeneration: A Mechanistic Continuum in Cerebral Small Vessel Disease and Dementia.
Eur J Neurosci
September 2025
Global Health Neurology Lab, Sydney, New South Wales, Australia.
Cerebral small vessel disease (CSVD) is a major yet underappreciated driver of cognitive impairment and dementia, contributing to nearly half of all cases. Emerging evidence indicates that CSVD is not merely a coexisting vascular condition but an active amplifier of neurodegeneration, operating through a self-perpetuating cascade of microvascular injury, blood-brain barrier (BBB) breakdown, and glymphatic system dysfunction. In this hypothesis-driven review, we propose the Integrated Vascular-Neurodegenerative Continuum, a mechanistic model in which vascular pathology triggers and accelerates neurodegeneration via intersecting pathways, including chronic cerebral hypoperfusion, oxidative stress, and APOE ε4-associated endothelial vulnerability.
View Article and Find Full Text PDFThe divergence between the central and peripheral vascular system, particularly the emergence of the blood-brain barrier (BBB), is central to the brain's homeostasis and functions. However, the molecular and genetic constituents that separating the BBB vascular cells from the rest remain elusive. Using single cell transcriptomics, we identified new cerebrovascular markers, e.
View Article and Find Full Text PDF