ArticleCell death & disease2022
Caveolin-1 identified as a key mediator of acute lung injury using bioinformatics and functional research.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- The role of fatty acid metabolism in acute lung injury: a special focus on immunometabolism.Cellular and molecular life sciences : CMLS · 2024Pooled it
- Impaired BCAA Catabolism Contributes To Acute Lung Injury By Triggering Oxidative Stress and Inflammatory Response Via the MAPK Pathway.Inflammation · 2026Article
- Cyclodextrin Inhibits Caveolin-1 to Regulate CD4Journal of immunology research · 2026Article
- Trained immunity attenuated acute lung injury by activating alveolar macrophages via AKT2-PDK1 axis-mediated metabolic reprogramming.Journal of translational medicine · 2025Article
- Senescent fibroblasts modulate the radiation response of neighboring epithelial cells.Cell death discovery · 2025Article
- bFGF Knockdown Inhibits mTOR Signaling by Suppressing Caveolin-1 and Aggravates Cognitive Damage After Arterial Ischemic Brain Injury in Juvenile Rats.Molecular neurobiology · 2025Article
- Caveolin-1 Is a Central Mediator of Acute Lung Injury in an Animal Model of Sickle Cell Disease.Pulmonary circulation · 2025Article
- The dual role of mTOR signaling in lung development and adult lung diseases.Cell & bioscience · 2025Review
- Development of an acute lung injury model for drug testing.Scientific reports · 2025Article
- The crosstalk of caveolin-1 and autophagy in different diseases.Frontiers in immunology · 2025Review
- Article
- Administration of turmeric kombucha ameliorates lipopolysaccharide-induced sepsis by attenuating inflammation and modulating gut microbiota.Frontiers in microbiology · 2024Article
- The critical roles of caveolin-1 in lung diseases.Frontiers in pharmacology · 2024Review
- Alveolar-capillary endocytosis and trafficking in acute lung injury and acute respiratory distress syndrome.Frontiers in immunology · 2024Review
- B2M is a Biomarker Associated With Immune Infiltration In High Altitude Pulmonary Edema.Combinatorial chemistry & high throughput screening · 2024Article
- Molecular markers of type II alveolar epithelial cells in acute lung injury by bioinformatics analysis.Scientific reports · 2023Article
- Review
- Aloe-Emodin Ameliorates Cecal Ligation and Puncture-Induced Sepsis.International journal of molecular sciences · 2023Article
- Qinhuo Shanggan oral solution resolves acute lung injury by down-regulating TLR4/NF-Frontiers in immunology · 2023Article
- The sirtuin family in health and disease.Signal transduction and targeted therapy · 2022Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute lung injury (ALI) is a potentially life-threatening, devastating disease with an extremely high rate of mortality. The underlying mechanism of ALI is currently unclear. In this study, we aimed to confirm the hub genes associated with ALI and explore their functions and molecular mechanisms using bioinformatics methods. Five microarray datasets available in GEO were used to perform Robust Rank Aggregation (RRA) to identify differentially expressed genes (DEGs) and the key genes were identified via the protein-protein interaction (PPI) network. Lipopolysaccharide intraperitoneal injection was administered to establish an ALI model. Overall, 40 robust DEGs, which are mainly involved in the inflammatory response, protein catabolic process, and NF-κB signaling pathway were identified. Among these DEGs, we identified two genes associated with ALI, of which the CAV-1/NF-κB axis was significantly upregulated in ALI, and was identified as one of the most effective targets for ALI prevention. Subsequently, the expression of CAV-1 was knocked down using AAV-shCAV-1 or CAV-1-siRNA to study its effect on the pathogenesis of ALI in vivo and in vitro. The results of this study indicated that CAV-1/NF-κB axis levels were elevated in vivo and in vitro, accompanied by an increase in lung inflammation and autophagy. The knockdown of CAV-1 may improve ALI. Mechanistically, inflammation was reduced mainly by decreasing the expression levels of CD3 and F4/80, and activating autophagy by inhibiting AKT/mTOR and promoting the AMPK signaling pathway. Taken together, this study provides crucial evidence that CAV-1 knockdown inhibits the occurrence of ALI, suggesting that the CAV-1/NF-κB axis may be a promising therapeutic target for ALI treatment.
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