ArticleNutrients2017
1α,25-dihydroxyvitamin D3 Attenuates TGF-β-Induced Pro-Fibrotic Effects in Human Lung Epithelial Cells through Inhibition of Epithelial-Mesenchymal Transition.
Article in Nutrients, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Vitamin D3-Deficient Diet Promotes Pulmonary Fibrosis Development in Murine Model of Hypersensitivity Pneumonitis.International journal of molecular sciences · 2025Article
- Aerosolized vitamin D attenuates ozone-induced inflammation and transcriptional responses via membrane antioxidant effects in human bronchial epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- The first step for understanding the molecular mechanism of the antifibrotic effect of inhaling 25(OH)-vitamin D3 and 1,25(OH)Frontiers in pharmacology · 2025Article
- Nutritional insights into pulmonary fibrosis: a comprehensive review on the impact of vitamins.Frontiers in nutrition · 2025Review
- Cellular and Molecular Genetic Mechanisms of Lung Fibrosis Development and the Role of Vitamin D: A Review.International journal of molecular sciences · 2024Review
- Involvement of the secosteroid vitamin D in autoimmune rheumatic diseases and COVID-19.Nature reviews. Rheumatology · 2023Review
- First Characterization of the Transcriptome of Lung Fibroblasts of SSc Patients and Healthy Donors of African Ancestry.International journal of molecular sciences · 2023Article
- Review
- Calcifediol for Use in Treatment of Respiratory Disease.Nutrients · 2022Review
- Association of vitamin D status with COVID-19 and its severity : Vitamin D and COVID-19: a narrative review.Reviews in endocrine & metabolic disorders · 2022Review
- The Role of Serum 1,25-Dihydroxy Vitamin D3 and PCT in Idiopathic Pulmonary Fibrosis.International journal of general medicine · 2022Article
- Fructose Induces Pulmonary Fibrotic Phenotype Through Promoting Epithelial-Mesenchymal Transition Mediated by ROS-Activated Latent TGF-β1.Frontiers in nutrition · 2022Article
- Article
- Vitamin D Endocrine System and COVID-19.JBMR plus · 2021Article
- Effect of supercritical carbon dioxide fluid extract from Chrysanthemum indicum Linné on bleomycin-induced pulmonary fibrosis.BMC complementary medicine and therapies · 2021Article
- Transforming growth factor beta 1 (TGFβ1) plasmatic levels and haplotype structures in obesity: a role for TGFβ1 in steatosis development.Molecular biology reports · 2021Article
- Downregulation of miR-17 suppresses TGF-β1-mediated renal fibrosis through targeting Smad7.Molecular and cellular biochemistry · 2021Article
- Fish Oil, Se Yeast, and Micronutrient-Enriched Nutrition as Adjuvant Treatment during Target Therapy in a Murine Model of Lung Cancer.Marine drugs · 2021Article
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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
Pulmonary fibrosis is a progressive fibrotic lung disease of persisting lung injury and ineffective wound repair, with poor prognosis. Epithelial-mesenchymal transition (EMT) of alveolar epithelia cells is an early event in the development of pulmonary fibrosis, and transforming growth factor β (TGF-β) is an acknowledged inducer of EMT. Epidemiological studies demonstrated that serum levels of 25-hydroxy-vitamin D were associated with the presence of fibrosis diseases. We investigated whether vitamin D attenuated TGF-β-induced pro-fibrotic effects through inhibiting EMT in human alveolar epithelia A549 cells. A549 cells were cultured with TGF-β alone or in combination with 1α,25-dihydroxyvitamin D3 (1α,25(OH)₂D₃). TGF-β increased the expression of the mesenchymal markers (N-cadherin and Vimentin), and decreased the expression of epithelial markers (E-cadherin). 1α,25(OH)₂D₃ attenuated these TGF-β-induced alterations. Furthermore, the EMT-related transcription factors (Snail and β-catenin) and the extracellular matrix genes (Collagen I and fibronectin) were inhibited by 1α,25(OH)₂D₃, while the expression of vitamin D receptor (VDR) was elevated. In addition, 1α,25(OH)₂D₃ alleviated the cell migration and the invasion abilities in TGF-β-stimulated A549 cells, determined by the scratch wound healing and transwell assays. Our findings suggested that 1α,25(OH)₂D₃ inhibited the pro-fibrotic phenotype of lung epithelial cells under TGF-β stimulation and provided new clues in the clinical management of pulmonary fibrosis.
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