ArticleCellular and molecular life sciences : CMLS2021
Metabolic regulation of RA macrophages is distinct from RA fibroblasts and blockade of glycolysis alleviates inflammatory phenotype in both cell types.
Article in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 57 citations in OpenAlex.
- Metabolic impact of low dose IL-2 therapy for primary Sjögren's Syndrome in a double-blind, randomized clinical trial.Clinical rheumatology · 2024Trial
- Review
- Targeting Glycolysis May Bridge Innate and Adaptive Immune Regulation in Experimental Peri-Implantitis.International journal of molecular sciences · 2026Article
- Review
- Ferroptosis-driven metabolic reprogramming in macrophages: Reshaping glucose utilization landscapes.Chinese medical journal · 2026Review
- Tofacitinib repairs inflammation and mitochondrial dysregulation in GM-CSF-reprogrammed RA macrophages.Cellular & molecular immunology · 2026Article
- The Oral-Gut-Immune-Nutrition Axis in Rheumatoid Arthritis: Molecular Mechanisms and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Rewiring immunity in rheumatoid arthritis: metabolic and epigenetic therapeutic strategies.Frontiers in pharmacology · 2026Review
- Telomerase-mediated immortalization preserves the anti-inflammatory activity of dental pulp stem cell extracellular vesicles.Frontiers in immunology · 2026Article
- Immunometabolism in rheumatoid arthritis: mechanisms, biomarkers, and the path to precision medicine.Frontiers in immunology · 2026Review
- PPP1R3B Suppresses Atherosclerosis by Promoting the M2 Polarization of Macrophages Through Glycogen Metabolic Reprogramming.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Histone lactylation promotes rheumatoid arthritis progression by increasing NFATc2 expression and the production of anti-lactylated histone autoantibodies.Nature communications · 2025Article
- Histone deacetylase 7 mediates lipopolysaccharide-inducible mitochondrial fission in macrophages.Journal of cell science · 2025Article
- The Glycolysis-HIF-1α axis induces IL-1β of macrophages in rheumatoid arthritis.Arthritis research & therapy · 2025Article
- Stimuli-responsive nanozymes for wound healing: From design strategies to therapeutic advances.Materials today. Bio · 2025Review
- Unveiling the Therapeutic Potential: Targeting Fibroblast-like Synoviocytes in Rheumatoid Arthritis.Expert reviews in molecular medicine · 2025Review
- Crossing the metabolic homeostasis divide: panoramic decoding of therapeutic targets for metabolic-inflammatory crosstalk in rheumatoid arthritis.Frontiers in immunology · 2025Review
- Targeting immune cell migration as therapy for inflammatory disease: a review.Frontiers in immunology · 2025Review
- Metabolic reprogramming: the central mechanism driving inflammatory polarization in rheumatoid arthritis and the regulatory role of traditional Chinese medicine.Frontiers in immunology · 2025Review
- Metabolic regulation of the immune system in health and diseases: mechanisms and interventions.Signal transduction and targeted therapy · 2024Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Recent studies have shown the significance of metabolic reprogramming in immune and stromal cell function. Yet, the metabolic reconfiguration of RA macrophages (MΦs) is incompletely understood during active disease and in crosstalk with other cell types in experimental arthritis. This study elucidates a distinct regulation of glycolysis and oxidative phosphorylation in RA MΦs compared to fibroblast (FLS), although PPP (Pentose Phosphate pathway) is similarly reconfigured in both cell types. 2-DG treatment showed a more robust impact on impairing the RA M1 MΦ-mediated inflammatory phenotype than IACS-010759 (IACS, complexli), by reversing ERK, AKT and STAT1 signaling, IRF8/3 transcription and CCL2 or CCL5 secretion. This broader inhibitory effect of 2-DG therapy on RA M1 MΦs was linked to dysregulation of glycolysis (GLUT1, PFKFB3, LDHA, lactate) and oxidative PPP (NADP conversion to NADPH), while both compounds were ineffective on oxidative phosphorylation. Distinctly, in RA FLS, 2-DG and IACS therapies constrained LPS/IFNγ-induced AKT and JNK signaling, IRF5/7 and fibrokine expression. Disruption of RA FLS metabolic rewiring by 2-DG or IACS therapy was accompanied by a reduction of glycolysis (HIF1α, PFKFB3) and suppression of citrate or succinate buildup. We found that 2-DG therapy mitigated CIA pathology by intercepting joint F480
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.