ArticleScientific reports2019
Caveolin-1 gene therapy inhibits inflammasome activation to protect from bleomycin-induced pulmonary fibrosis.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- A gene therapy approach to prevent dilated intercellular space, a hallmark of gastroesophageal reflux disease.Gene therapy · 2026Article
- Cyclodextrin Inhibits Caveolin-1 to Regulate CD4Journal of immunology research · 2026Article
- Bioinformatics and experimental animal model reveal the prognostic value of immunogenic cell death-related proteins in idiopathic pulmonary fibrosis.Journal of thoracic disease · 2025Article
- Role of membrane microdomains in cardiac protection: strategies for diabetic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2025Review
- Regulation of the terminal complement cascade in adipose tissue for control of its volume, cellularity, and fibrosis.Obesity (Silver Spring, Md.) · 2025Review
- Article
- Ratio of miRNA-29 to miRNA-199 expression coordinates mesenchymal stem cell repair of bleomycin-induced pulmonary injury.Molecular therapy. Nucleic acids · 2025Article
- The critical roles of caveolin-1 in lung diseases.Frontiers in pharmacology · 2024Review
- A spatial sequencing atlas of age-induced changes in the lung during influenza infection.Nature communications · 2023Article
- Suppression of NLRP3 inflammasome by ivermectin ameliorates bleomycin-induced pulmonary fibrosis.Journal of Zhejiang University. Science. B · 2023Article
- Machine learning identified MDK score has prognostic value for idiopathic pulmonary fibrosis based on integrated bulk and single cell expression data.Frontiers in genetics · 2023Article
- Caveolin-1 in vascular health and glaucoma: A critical vascular regulator and potential therapeutic target.Frontiers in medicine · 2023Review
- The Aging Human Lung Mucosa: A Proteomics Study.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022Article
- Caveolin-1 negatively regulates inflammation and fibrosis in silicosis.Journal of cellular and molecular medicine · 2022Article
- CAV1 is a prognostic predictor for patients with idiopathic pulmonary fibrosis and lung cancer.Journal of biosciences · 2022Article
- Critical Role of Caveolin-1 Loss/Dysfunction in Pulmonary Hypertension.Medical sciences (Basel, Switzerland) · 2021Review
- ER-anchored CRTH2 antagonizes collagen biosynthesis and organ fibrosis via binding LARP6.The EMBO journal · 2021Article
- Inflammasome Genetic Variants, Macrophage Function, and Clinical Outcomes in Cystic Fibrosis.American journal of respiratory cell and molecular biology · 2021Observational
- Pulmonary gene delivery-Realities and possibilities.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Bioinformatics Analysis Identifies Potential Ferroptosis Key Genes in the Pathogenesis of Pulmonary Fibrosis.Frontiers in genetics · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a devastating and fatal disease and characterized by increased deposition of extracellular matrix proteins and scar formation in the lung, resulting from alveolar epithelial damage and accumulation of inflammatory cells. Evidence suggests that Caveolin-1 (Cav-1), a major component of caveolae which regulates cell signaling and endocytosis, is a potential target to treat fibrotic diseases, although the mechanisms and responsible cell types are unclear. We show that Cav-1 expression was downregulated both in alveolar epithelial type I cells in bleomycin-injured mouse lungs and in lung sections from IPF patients. Increased expression of IL-1β and caspase-1 has been observed in IPF patients, indicating inflammasome activation associated with IPF. Gene transfer of a plasmid expressing Cav-1 using transthoracic electroporation reduced infiltration of neutrophils and monocytes/macrophages and protected from subsequent bleomycin-induced pulmonary fibrosis. Overexpression of Cav-1 suppressed bleomycin- or silica-induced activation of caspase-1 and maturation of pro-IL-1β to secrete cleaved IL-1β both in mouse lungs and in primary type I cells. These results demonstrate that gene transfer of Cav-1 downregulates inflammasome activity and protects from subsequent bleomycin-mediated pulmonary fibrosis. This indicates a pivotal regulation of Cav-1 in inflammasome activity and suggests a novel therapeutic strategy for patients with IPF.
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