ArticleJournal of translational medicine2023
Mitochondrial folate pathway regulates myofibroblast differentiation and silica-induced pulmonary fibrosis.
Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Research on the role and mechanism of SLC7A5 in idiopathic pulmonary fibrosis.Molecular medicine reports · 2026Article
- Folate metabolism-related gene signature reveals prognostic and immunological characteristics in idiopathic pulmonary fibrosis.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2026Article
- Article
- MTHFD2: a promising metabolic checkpoint for diseases.Journal of translational medicine · 2026Review
- Oxidative Stress Biomarkers in Silicosis: A Systematic Review.Diseases (Basel, Switzerland) · 2026Review
- Bleomycin-induced lung fibrosis and dysfunction is exacerbated by G6PD deficiency.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Tools of the trade: leveraging 3DFrontiers in pharmacology · 2026Review
- Apoptotic Bodies Restore NAD and Mitochondrial Homeostasis in Fibroblasts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Nutritional insights into pulmonary fibrosis: a comprehensive review on the impact of vitamins.Frontiers in nutrition · 2025Review
- Multi-omics and multi-stages integration identified a novel variant associated with silicosis risk.Archives of toxicology · 2024Article
- Article
- Integration of apaQTL and eQTL analysis reveals novel SNPs associated with occupational pulmonary fibrosis risk.Archives of toxicology · 2024Article
- Redox Pathogenesis in Rheumatic Diseases.ACR open rheumatology · 2024Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSilica-induced pulmonary fibrosis (silicosis) is a diffuse interstitial fibrotic disease characterized by the massive deposition of extracellular matrix in lung tissue. Fibroblast to myofibroblast differentiation is crucial for the disease progression. Inhibiting myofibroblast differentiation may be an effective way for pulmonary fibrosis treatment.
methodsThe experiments were conducted in TGF-β treated human lung fibroblasts to induce myofibroblast differentiation in vitro and silica treated mice to induce pulmonary fibrosis in vivo.
resultsBy quantitative mass spectrometry, we revealed that proteins involved in mitochondrial folate metabolism were specifically upregulated during myofibroblast differentiation following TGF-β stimulation. The expression level of proteins in mitochondrial folate pathway, MTHFD2 and SLC25A32, negatively regulated myofibroblast differentiation. Moreover, plasma folate concentration was significantly reduced in patients and mice with silicosis. Folate supplementation elevated the expression of MTHFD2 and SLC25A32, alleviated oxidative stress and effectively suppressed myofibroblast differentiation and silica-induced pulmonary fibrosis in mice.
conclusionOur study suggests that mitochondrial folate pathway regulates myofibroblast differentiation and could serve as a potential target for ameliorating silica-induced pulmonary fibrosis.
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