ArticleInternational journal of molecular sciences2018
Fenofibrate Reduces the Asthma-Related Fibroblast-To-Myofibroblast Transition by TGF-Β/Smad2/3 Signaling Attenuation and Connexin 43-Dependent Phenotype Destabilization.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- [Pathological roles of lipid metabolism disorders in asthma and related intervention strategies].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Review
- Role of alternative oral therapy for the management of wet age-related macular degeneration and proliferative diabetic retinopathy.World journal of diabetes · 2025Review
- Qufeng Jiejing formula ameliorated the injury of airway smooth muscle cells induced by platelet-derived growth factor-BB through the transforming growth factor-β1/Smads signaling pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Fenofibrate suppressesFrontiers in cellular and infection microbiology · 2025Article
- Silencing SMAD4 inhibits inflammation and ferroptosis in asthma by blocking the IL-17A signaling pathway.Respiratory research · 2024Article
- Hypoxia enhances anti-fibrotic properties of extracellular vesicles derived from hiPSCs via the miR302b-3p/TGFβ/SMAD2 axis.BMC medicine · 2023Article
- PPARδ Agonist GW501516 Suppresses the TGF-β-Induced Profibrotic Response of Human Bronchial Fibroblasts from Asthmatic Patients.International journal of molecular sciences · 2023Article
- Anti-Inflammatory Effects of Lipid-Lowering Drugs and Supplements-A Narrative Review.Nutrients · 2023Review
- The miR-124-3p regulates the allergic airway inflammation and remodeling in an ovalbumin-asthmatic mouse model by inhibiting S100A4.Immunity, inflammation and disease · 2023Article
- Article
- SB203580-A Potent p38 MAPK Inhibitor Reduces the Profibrotic Bronchial Fibroblasts Transition Associated with Asthma.International journal of molecular sciences · 2021Article
- Adiponectin and Asthma: Knowns, Unknowns and Controversies.International journal of molecular sciences · 2021Review
- Responsiveness of human bronchial fibroblasts and epithelial cells from asthmatic and non-asthmatic donors to the transforming growth factor-βBMC molecular and cell biology · 2021Article
- Targeting Airway Smooth Muscle Hypertrophy in Asthma: An Approach Whose Time Has Come.Journal of asthma and allergy · 2021Review
- Peroxisome Proliferator-Activated Receptors as a Therapeutic Target in Asthma.PPAR research · 2020Review
- Fenofibrate Inhibits Subretinal Fibrosis Through Suppressing TGF-β-Smad2/3 signaling and Wnt signaling in Neovascular Age-Related Macular Degeneration.Frontiers in pharmacology · 2020Article
- Fungal and bacterial microbiome dysbiosis and imbalance of trans-kingdom network in asthma.Clinical and translational allergy · 2020Article
- Resolution of allergic asthma.Seminars in immunopathology · 2019Review
- Connexin 43 plays an important role in the transformation of cholangiocytes with Clonochis sinensis excretory-secretory protein and N-nitrosodimethylamine.PLoS neglected tropical diseases · 2019Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The activation of human bronchial fibroblasts by transforming growth factor-β₁ (TGF-β₁) leads to the formation of highly contractile myofibroblasts in the process of the fibroblast⁻myofibroblast transition (FMT). This process is crucial for subepithelial fibrosis and bronchial wall remodeling in asthma. However, this process evades current therapeutic asthma treatment strategies. Since our previous studies showed the attenuation of the TGF-β₁-induced FMT in response to lipid-lowering agents (e.g., statins), we were interested to see whether a corresponding effect could be obtained upon administration of hypolipidemic agents. In this study, we investigated the effect of fenofibrate on FMT efficiency in populations of bronchial fibroblasts derived from asthmatic patients. Fenofibrate exerted a dose-dependent inhibitory effect on the FMT, even though it did not efficiently affect the expression of α-smooth muscle actin (α-SMA; marker of myofibroblasts); however, it considerably reduced its incorporation into stress fibers through connexin 43 regulation. This effect was accompanied by disturbances in the actin cytoskeleton architecture, impairments in the maturation of focal adhesions, and the fenofibrate-induced deactivation of TGF-β₁/Smad2/3 signaling. These data suggest that fenofibrate interferes with myofibroblastic differentiation during asthma-related subepithelial fibrosis. The data indicate the potential application of fenofibrate in the therapy and prevention of bronchial remodeling during the asthmatic process.
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