ArticleCellular and molecular life sciences : CMLS2024
LPS-induced monocarboxylate transporter-1 inhibition facilitates lactate accumulation triggering epithelial-mesenchymal transformation and pulmonary fibrosis.
Article in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Integrative transcriptomic and bioinformatic analyses predict candidate EMT-related genes in sepsis-associated acute lung injury.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Lactate metabolism and lactylation in cancer: from pathogenesis to therapeutic advances.Signal transduction and targeted therapy · 2026Review
- Preventive Effects of Probiotic Formula on Metabolic Stress Associated Physical Fatigue in Forced Swimming and LPS-Induced Mouse Models.Journal of microbiology and biotechnology · 2026Article
- Lactate derived from macrophages drives skin dermal fibroblasts phenotypic remodeling via MCT1-primed histone H3 lysine 23 lactylation in hypertrophic scar.Nature communications · 2026Article
- Lactate and lactylation in sepsis: regulation of immune-metabolic crosstalk and organ injury.Frontiers in immunology · 2026Review
- Glycolysis to lactylation: Unraveling the metabolic and epigenetic landscape in tissue fibrosis (Review).Molecular medicine reports · 2025Review
- Succinic Acid-Induced Macrophage Endocytosis Promotes Extracellular Vesicle-Based Integrin Beta1 Transfer Accelerating Fibroblast Activation and Sepsis-Associated Pulmonary Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Lactate and Lactylation in Respiratory Diseases: from Molecular Mechanisms to Targeted Strategies.Lung · 2025Review
- Lactate and lactylation: novel perspectives on fibrosis pathogenesis and therapeutic directions.Journal of translational medicine · 2025Review
- Eno1 in sepsis-induced coagulopathy: a pleiotropic mechanism hypothesis involving immunomodulation and endothelial dysfunction.Thrombosis journal · 2025Article
- Regulator of cullins-1 predicts a poor prognosis and regulates epithelial-mesenchymal transition process through GSK-3β/Wnt signaling in renal cell carcinoma.Translational andrology and urology · 2025Article
- Inhibition of Lactate Accumulation via USP38-Mediated MCT1 Deubiquitination Activates AKT/mTOR Signaling to Mitigate PM2.5-Induced Lung Injury.Journal of clinical laboratory analysis · 2025Article
- Pyruvate kinase M2 modulates mitochondrial dynamics and EMT in alveolar epithelial cells during sepsis-associated pulmonary fibrosis.Journal of translational medicine · 2025Article
- Epithelial-mesenchymal transition in pulmonary fibrosis: molecular mechanisms and emerging therapeutic strategies.Frontiers in medicine · 2025Review
- Targeting alveolar epithelial cell metabolism in pulmonary fibrosis: Pioneering an emerging therapeutic strategy.Frontiers in cell and developmental biology · 2025Review
- Unlocking the secrets of glucose metabolism reprogramming: the role in pulmonary diseases.Frontiers in pharmacology · 2025Review
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9 authors.
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Abstract
The epithelial-mesenchymal transformation (EMT) process of alveolar epithelial cells is recognized as involved in the development of pulmonary fibrosis. Recent evidence has shown that lipopolysaccharide (LPS)-induced aerobic glycolysis of lung tissue and elevated lactate concentration are associated with the pathogenesis of sepsis-associated pulmonary fibrosis. However, it is uncertain whether LPS promotes the development of sepsis-associated pulmonary fibrosis by promoting lactate accumulation in lung tissue, thereby initiating EMT process. We hypothesized that monocarboxylate transporter-1 (MCT1), as the main protein for lactate transport, may be crucial in the pathogenic process of sepsis-associated pulmonary fibrosis. We found that high concentrations of lactate induced EMT while moderate concentrations did not. Besides, we demonstrated that MCT1 inhibition enhanced EMT process in MLE-12 cells, while MCT1 upregulation could reverse lactate-induced EMT. LPS could promote EMT in MLE-12 cells through MCT1 inhibition and lactate accumulation, while this could be alleviated by upregulating the expression of MCT1. In addition, the overexpression of MCT1 prevented LPS-induced EMT and pulmonary fibrosis in vivo. Altogether, this study revealed that LPS could inhibit the expression of MCT1 in mouse alveolar epithelial cells and cause lactate transport disorder, which leads to lactate accumulation, and ultimately promotes the process of EMT and lung fibrosis.
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