ArticleMatrix biology : journal of the International Society for Matrix Biology2011
Caveolin-1 modulates TGF-β1 signaling in cardiac remodeling.
Article in Matrix biology : journal of the International Society for Matrix Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.
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Who cites it
36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 59 citations in OpenAlex.
- Genomic data-driven framework for drug target discovery in atrial fibrillation.Journal of translational medicine · 2025Pooled it
- Association Between Rs3807989 Polymorphism in Caveolin-1 (CAV1) Gene and Atrial Fibrillation: A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2016Pooled it
- Article
- Cav-1 deficiency induces cardiac dysfunction via the AdipoR1-AMPK-mTOR autophagy pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Protective Effects of Low-Intensity Pulsed Ultrasound on Cardiac Electrophysiological Function in a Rat Model of Ischemic Cardiomyopathy.Journal of the American Heart Association · 2025Article
- Genetic Manipulation of Caveolin-1 in a Transgenic Mouse Model of Aortic Root Aneurysm: Sex-Dependent Effects on Endothelial and Smooth Muscle Function.International journal of molecular sciences · 2024Article
- Caveolin-1-Derived Peptide Reduces ER Stress and Enhances Gelatinolytic Activity in IPF Fibroblasts.International journal of molecular sciences · 2022Article
- New Insights into Pathomechanisms and Treatment Possibilities for Lung Silicosis.International journal of molecular sciences · 2021Review
- Emerging cellular and molecular determinants of idiopathic pulmonary fibrosis.Cellular and molecular life sciences : CMLS · 2021Review
- Endothelial cells and endothelial progenitor cells in the pathogenesis of systemic sclerosis.European journal of rheumatology · 2020Review
- MG53/CAV1 regulates transforming growth factor-β1 signaling-induced atrial fibrosis in atrial fibrillation.Cell cycle (Georgetown, Tex.) · 2020Article
- Loss of Caveolin-1 and caveolae leads to increased cardiac cell stiffness and functional decline of the adult zebrafish heart.Scientific reports · 2020Article
- Caveolin-1 gene therapy inhibits inflammasome activation to protect from bleomycin-induced pulmonary fibrosis.Scientific reports · 2019Article
- Understanding cardiac extracellular matrix remodeling to develop biomarkers of myocardial infarction outcomes.Matrix biology : journal of the International Society for Matrix Biology · 2019Review
- Value of multilocus genetic risk score for atrial fibrillation in end-stage kidney disease patients in a Polish population.Scientific reports · 2018Article
- Caveolin-1 Scaffolding Domain Peptides Alleviate Liver Fibrosis by Inhibiting TGF-β1/Smad Signaling in Mice.International journal of molecular sciences · 2018Article
- Suppression of angiotensin II-induced pathological changes in heart and kidney by the caveolin-1 scaffolding domain peptide.PloS one · 2018Article
- Snail1 is positively correlated with atrial fibrosis in patients with atrial fibrillation and rheumatic heart disease.Experimental and therapeutic medicine · 2017Article
- TGF-β-Induced Endothelial-Mesenchymal Transition in Fibrotic Diseases.International journal of molecular sciences · 2017Review
- Transforming growth factor β: A potential biomarker and therapeutic target of ventricular remodeling.Oncotarget · 2017Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The cardiac response to myocardial injury includes fibrotic and hypertrophic processes and a key mediator in this response is transforming growth factor-β1 (TGF-β1). Caveolin-1 (cav1), the main structural protein of caveolae, is an inhibitor of the TGF-β1 signaling pathway. To examine the role of cav1 in cardiac repair, cav1 deficient (Cav1(-/-)) and wild type (WT) mice were subjected to cryoinjury of the left ventricle (LV). At baseline the two groups exhibited no inflammation, similar collagen content, and similar cardiac function. After injury, Cav1(-/-) animals displayed enhanced TGF-β1 signaling, as reflected by a 3-fold increase in the activation of the Smad2-dependent pathway and more widespread collagen deposition in the heart. Qualitative and quantitative analyses indicated that collagen deposition peaked in the WT LV 14days after injury, accompanied by increased mRNA abundance for procol1a2 (2-fold) and procol3a1 (3-fold). Collagen deposition was further enhanced in Cav1(-/-) mice, which was accompanied by reduced expression of matrix metalloproteinases MMP-8 (3-fold) and -13 mRNA (2-fold). The levels of expression of inflammatory markers of acute phase were similar between the strains However, macrophage clearance in the damaged region was delayed in Cav1(-/-) mice. We observed a 4-fold decrease in collagen deposition in Cav1(-/-) mice injected with a cav1 scaffolding domain peptide (CSD) and a 2-fold decrease in WT mice treated with the CSD. We conclude that cav1 has a direct role in reducing TGF-β1 signaling and as such might be an appropriate target for therapies to influence cardiac remodeling.
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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.