ArticleAmerican journal of physiology. Lung cellular and molecular physiology2008
The role of caveolin-1 in pulmonary matrix remodeling and mechanical properties.
Article in American journal of physiology. Lung cellular and molecular physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 60 citations in OpenAlex.
- Cigarette smoke enhances proliferation and extracellular matrix deposition by human fetal airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2014Trial
- Loss ofLife (Basel, Switzerland) · 2025Article
- Sex-dependent influence of LMAN1 on allergen-induced airway hyperresponsiveness.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- The vascular phenotype of BPD: new basic science insights-new precision medicine approaches.Pediatric research · 2024Review
- Article
- Paradoxical Changes: EMMPRIN Tissue and Plasma Levels in Marfan Syndrome-Related Thoracic Aortic Aneurysms.Journal of clinical medicine · 2024Article
- The critical roles of caveolin-1 in lung diseases.Frontiers in pharmacology · 2024Review
- Epithelial coxsackievirus adenovirus receptor promotes house dust mite-induced lung inflammation.Nature communications · 2022Article
- NOD2 Signaling Circuitry during Allergen Sensitization Does Not Worsen Experimental Neutrophilic Asthma but Promotes a Th2/Th17 Profile in Asthma Patients but Not Healthy Subjects.International journal of molecular sciences · 2022Article
- Critical Role of Caveolin-1 Loss/Dysfunction in Pulmonary Hypertension.Medical sciences (Basel, Switzerland) · 2021Review
- MYOC Promotes the Differentiation of C2C12 Cells by Regulation of the TGF-β Signaling Pathways via CAV1.Biology · 2021Article
- The Caveolin-1 Scaffolding Domain Peptide Reverses Aging-Associated Deleterious Changes in Multiple Organs.The Journal of pharmacology and experimental therapeutics · 2021Article
- Arterial Wall Stiffening in Caveolin-1 Deficiency-Induced Pulmonary Artery Hypertension in Mice.Experimental mechanics · 2021Article
- Crosstalk between mechanotransduction and metabolism.Nature reviews. Molecular cell biology · 2021Review
- Signaling Pathways Involved in the Development of Bronchopulmonary Dysplasia and Pulmonary Hypertension.Children (Basel, Switzerland) · 2020Review
- Adipose-derived mesenchymal stromal/stem cells in systemic sclerosis: Alterations in function and beneficial effect on lung fibrosis are regulated by caveolin-1.Journal of scleroderma and related disorders · 2019Article
- In vitro effect of caveolin-1 as a slow-release material on bone-tendon junction healing: A comparative study.The Kaohsiung journal of medical sciences · 2019Article
- Frontline Science: RIP2 promotes house dust mite-induced allergic airway inflammation.Journal of leukocyte biology · 2018Article
- Potential contribution of alveolar epithelial type I cells to pulmonary fibrosis.Bioscience reports · 2017Review
- TRIM72 modulates caveolar endocytosis in repair of lung cells.American journal of physiology. Lung cellular and molecular physiology · 2016Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Caveolin-1 (cav1) is a 22-kDa membrane protein essential to the formation of small invaginations in the plasma membrane, called caveolae. The cav1 gene is expressed primarily in adherent cells such as endothelial and smooth muscle cells and fibroblasts. Caveolae contain a variety of signaling receptors, and cav1 notably downregulates transforming growth factor (TGF)-beta signal transduction. In pulmonary pathologies such as interstitial fibrosis or emphysema, altered mechanical properties of the lungs are often associated with abnormal ECM deposition. In this study, we examined the physiological functions and the deposition of ECM in cav1(-/-) mice at various ages (1-12 mo). Cav1(-/-) mice lack caveolae and by 3 mo of age have significant reduced lung compliance and increased elastance and airway resistance. Pulmonary extravasation of fluid, as part of the cav1(-/-) mouse phenotype, probably contributed to the alteration of compliance, which was compounded by a progressive increase in deposition of collagen fibrils in airways and parenchyma. We also found that the increased elastance was caused by abundant elastic fiber deposition primarily around airways in cav1(-/-) mice at least 3 mo old. These observed changes in the ECM composition probably also contribute to the increased airway resistance. The higher deposition of collagen and elastic fibers was associated with increased tropoelastin and col1alpha2 and col3alpha1 gene expression in lung tissues, which correlated tightly with increased TGF-beta/Smad signal transduction. Our study illustrates that perturbation of cav1 function may contribute to several pulmonary pathologies as the result of the important role played by cav1, as part of the TGF-beta signaling pathway, in the regulation of the pulmonary ECM.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.