ArticleNature communications2025
Mitochondrial one-carbon metabolism is required for TGF-β-induced glycine synthesis and fibrotic responses.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Mitochondrial Dysfunction: From Molecular Mechanisms to Modern Approaches for Basic and Clinical Research.Biomedicines · 2026Review
- Metabolic changes and plasma glycine predict the risk of acute cellular rejection in heart transplantation.JTCVS open · 2026Article
- Targeting Inhibin Enhances Wagyu Oocyte Competence and Embryo Quality: A Comparative Study of In Vivo Immunization and In Vitro Antibody Supplementation.Antioxidants (Basel, Switzerland) · 2026Article
- Article
- Serum metabolic characteristics of interstitial lung disease: a potential link between endocrine aging and gut-derived metabolites.Frontiers in medicine · 2026Article
- GPX7 marks fibroblast-associated stromal-innate immune crosstalk in ulcerative colitis.Frontiers in immunology · 2026Article
- The effects of combined low-dose cadmium and deltamethrin on mitochondrial bioenergetics and metabolism in human lung fibroblasts.Toxicology reports · 2025Article
- Metabolic control of collagen synthesis.Matrix biology : journal of the International Society for Matrix Biology · 2024Review
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17 authors.
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Abstract
TGF-β-dependent activation of lung fibroblasts is a hallmark of Idiopathic Pulmonary Fibrosis (IPF) which results in excessive collagen deposition and progressive scarring. Collagen production by lung fibroblasts is supported by de novo synthesis of glycine, the most abundant amino acid in collagen protein. SHMT2 produces glycine by transferring a one-carbon (1 C) unit from serine to tetrahydrofolate (THF), producing 5,10-methylene-THF (meTHF). meTHF is then converted back to THF in the mitochondrial 1 C pathway. It is unknown how 1 C metabolism contributes to collagen protein production and fibrosis. Here, we demonstrate that TGF-β induces the expression of mitochondrial 1 C pathway enzymes, including MTHFD2, in human lung fibroblasts. MTHFD2 was required for TGF-β-induced cellular glycine accumulation and collagen protein production in lung fibroblasts. Pharmacologic inhibition of MTHFD2 ameliorated fibrotic responses after intratracheal bleomycin instillation in vivo. Our findings suggest that mitochondrial 1 C metabolism is a therapeutic target for IPF and other fibrotic diseases.
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