ArticleJournal of thoracic disease2014
Hypoxia induces cardiac fibroblast proliferation and phenotypic switch: a role for caveolae and caveolin-1/PTEN mediated pathway.
Article in Journal of thoracic disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 50 citations in OpenAlex.
- Role of Anti-Inflammatory and Antioxidant Properties of Natural Products in Curing Cardiovascular Diseases.Current issues in molecular biology · 2025Review
- The endogenous glutamatergic transmitter system promotes collagen synthesis in cardiac fibroblasts under hypoxia.Frontiers in cardiovascular medicine · 2025Article
- Enhanced neoangiogenesis and balance of the immune response mediated by the Wilms' tumor suppressor WT1 favor repair after myocardial infarction.Theranostics · 2025Article
- Hypoxic-Normoxic Crosstalk Activates Pro-Inflammatory Signaling in Human Cardiac Fibroblasts and Myocytes in a Post-Infarct Myocardium on a Chip.Advanced healthcare materials · 2024Article
- Epigenetic Regulation in Myocardial Fibroblasts and Its Impact on Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Distinct phenotypes induced by acute hypoxia and TGF-β1 in human adult cardiac fibroblasts.Journal of molecular and cellular cardiology plus · 2024Article
- CAV1 Protein Encapsulated in Mouse BMSC-Derived Extracellular Vesicles Alleviates Myocardial Fibrosis Following Myocardial Infarction by Blocking the TGF-β1/SMAD2/c-JUN Axis.Journal of cardiovascular translational research · 2024Article
- The purified extract of steamedJournal of ginseng research · 2023Article
- Identification of Adamts4 as a novel adult cardiac injury biomarker with therapeutic implications in patients with cardiac injuries.Scientific reports · 2022Article
- Knockdown of miR-214 Alleviates Renal Interstitial Fibrosis by Targeting the Regulation of the PTEN/PI3K/AKT Signalling Pathway.Oxidative medicine and cellular longevity · 2022Article
- Characterization and Validation of ceRNA-Mediated Pathway-Pathway Crosstalk Networks Across Eight Major Cardiovascular Diseases.Frontiers in cell and developmental biology · 2022Article
- Metabolic dysfunction and inflammatory disease: the role of stromal fibroblasts.The FEBS journal · 2021Review
- MicroRNA expression profiling involved in doxorubicin-induced cardiotoxicity using high-throughput deep-sequencing analysis.Oncology letters · 2021Article
- Yes-Associated Protein (Yap) Is Up-Regulated in Heart Failure and Promotes Cardiac Fibroblast Proliferation.International journal of molecular sciences · 2021Article
- Mechanical Strain Regulates Myofibroblast Differentiation of Human Scleral Fibroblasts by YAP.Frontiers in physiology · 2021Article
- Engineering the Cellular Microenvironment of Post-infarct Myocardium on a Chip.Frontiers in cardiovascular medicine · 2021Review
- Regulation of left atrial fibrosis induced by mitral regurgitation by SIRT1.Scientific reports · 2020Article
- Rhein, a novel Histone Deacetylase (HDAC) inhibitor with antifibrotic potency in human myocardial fibrosis.Scientific reports · 2020Article
- Article
- Role of Caveolin-1 in Diabetes and Its Complications.Oxidative medicine and cellular longevity · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCardiac fibrosis following myocardial infarction (MI) results in heart failure. Caveolin-1, the main structural protein of caveolae, regulates signal transduction pathways controlling cell proliferation and apoptosis. Meanwhile, low phosphatase and tensin homolog (PTEN) activity enhances the PI3K/Akt signal pathway to induce cell proliferation. But whether caveolin-1 and PTEN activation regulates cardiac fibroblast proliferation and contributes to cardiac fibrosis from ischemic injury is incompletely understood. This study investigates whether hypoxia inducing cardiac fibroblast proliferation and phenotypic switch is caveolin-dependent.
methodsWe used in vitro and in vivo models of ischemic injury, immunohistochemical staining, and cell proliferation assays to address this hypothesis.
resultsWe found that MI induced collagen deposition and cardiac dysfunction. After MI, mice displayed reduced caveolin-1 and PTEN expression and increased α-smooth muscle actin (α-SMA) expression in the infarct zone. Qualitative and quantitative analyses indicated that caveolin-1 expression was lowest at 7 days after MI, accompanied by increased collagen deposition and attenuated cardiac function. We cultured cardiac fibroblasts of mice were in hypoxia or normoxia conditions for 12, 24 and 48 hours. At all the time points, caveolin-1 and PTEN expression were gradually reduced, whereas, α-SMA was gradually increased. We also observed that cell viability was increased at 12 and 24 h after hypoxia then lightly decreased at 48 h. Additionally, disruption of caveolae with methyl-β-cyclodextrin (MβCD) enhanced p-Akt and α-SMA expression and fibroblast proliferation and phenotypic switch.
conclusionsThese findings suggest a key role for caveolae, perhaps through the caveolin-1/PTEN signaling pathway, in cardiac fibroblast proliferation and phenotypic switch under hypoxia.
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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.