ArticleCell death & disease2023
Airway epithelial cGAS inhibits LPS-induced acute lung injury through CREB signaling.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Spotlight on cGAS-STING: role in disease pathogenesis and therapeutic potential.Molecular biomedicine · 2026Review
- YOD1 promotes ferroptosis in acute lung injury by deubiquitination of NCOA4.Communications biology · 2025Article
- Bridging dimensions: a comparative analysis of 2D and 3D in vitro models for hepatocellular carcinoma research.Archives of toxicology · 2025Article
- MERS-CoV and SARS-CoV-2 infection in diverse human lung organoid-derived cultures.Journal of virology · 2025Article
- Baicalin inhibits LPS-induced apoptosis and inflammation in WI- 38 cells by promoting FOXA2/TRIM27 Interaction: Implications for pediatric pneumonia mechanisms.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Optimization, Characterization and Pharmacological Validation of the Endotoxin-Induced Acute Pneumonitis Mouse Model.Biomedicines · 2025Article
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
Abstract
Increased levels of cytosolic DNA in lung tissues play an important role in acute lung injury. However, the detailed mechanisms involved remain elusive. Here, we found that cyclic GMP-AMP synthase (cGAS, a cytosolic DNA sensor) expression was increased in airway epithelium in response to increased cytosolic DNA. Conditional deletion of airway epithelial cGAS exacerbated acute lung injury in mice, cGAS knockdown augmented LPS-induced production of interleukin (IL)-6 and IL-8. Mechanically, deletion of cGAS augmented expression of phosphorylated CREB (cAMP response element-binding protein), and cGAS directly interacted with CREB via its C-terminal domain. Furthermore, CREB knockdown rescued the LPS-induced excessive inflammatory response caused by cGAS deletion. Our study demonstrates that airway epithelial cGAS plays a protective role in acute lung injury and confirms a non-canonical cGAS-CREB pathway that regulates the inflammatory responses in airway epithelium to mediate LPS-induced acute lung injury.
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Registered trials
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