ArticleAnnals of the New York Academy of Sciences2012
Roles for claudins in alveolar epithelial barrier function.
Article in Annals of the New York Academy of Sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 61 citations in OpenAlex.
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- Airway Epithelium: A Neglected but Crucial Cell Type in Asthma Pathobiology.Diagnostics (Basel, Switzerland) · 2023Review
- Dysfunction of epithelial permeability barrier induced by HMGB1 in 2.5D cultures of human epithelial cells.Tissue barriers · 2022Review
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- Loss of SOX18/CLAUDIN5 disrupts the pulmonary endothelial barrier in ventilator-induced lung injury.Frontiers in physiology · 2022Article
- Permeability Properties of anCellular and molecular bioengineering · 2021Article
- Lung Cancer Models Reveal Severe Acute Respiratory Syndrome Coronavirus 2-Induced Epithelial-to-Mesenchymal Transition Contributes to Coronavirus Disease 2019 Pathophysiology.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2021Article
- Deficiency of lung-specific claudin-18 leads to aggravated infection with Cryptococcus deneoformans through dysregulation of the microenvironment in lungs.Scientific reports · 2021Article
- Effects of histone deacetylase inhibitors Tricostatin A and Quisinostat on tight junction proteins of human lung adenocarcinoma A549 cells and normal lung epithelial cells.Histochemistry and cell biology · 2021Article
- Characteristics of Passive Solute Transport across Primary Rat Alveolar Epithelial Cell Monolayers.Membranes · 2021Article
- SPAK-p38 MAPK signal pathway modulates claudin-18 and barrier function of alveolar epithelium after hyperoxic exposure.BMC pulmonary medicine · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Terminal airspaces of the lung, alveoli, are sites of gas exchange that are sensitive to disrupted fluid balance. The alveolar epithelium is a heterogeneous monolayer of cells interconnected by tight junctions at sites of cell-cell contact. Paracellular permeability depends on claudin (cldn)-family tight junction proteins. Of over a dozen alveolar cldns, cldn-3, cldn-4, and cldn-18 are the most highly expressed; other prominent alveolar claudins include cldn-5 and cldn-7. Cldn-3 is primarily expressed by type II alveolar epithelial cells, whereas cldn-4 and cldn-18 are expressed throughout the alveolar epithelium. Lung diseases associated with pulmonary edema, such as alcoholic lung syndrome and acute lung injury, affect alveolar claudin expression, which is frequently associated with impaired fluid clearance due to increased alveolar leak. However, recent studies have identified a role for increased cldn-4 in protecting alveolar barrier function following injury. Thus, alveolar claudins are dynamically regulated, tailoring lung barrier function to control the air-liquid interface.
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Registered trials
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