ArticleScientific reports2017
Resolution of TLR2-induced inflammation through manipulation of metabolic pathways in Rheumatoid Arthritis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 78 citations in OpenAlex.
- Rheumatoid arthritis synovial microenvironment induces metabolic and functional adaptations in dendritic cells.Clinical and experimental immunology · 2020Trial
- Long Non-Coding RNAsCurrent issues in molecular biology · 2026Article
- Discovery of Novel NMR-Based Biomarkers and Interpretable Machine Learning Models for Risk Prediction of Rheumatoid Arthritis.Metabolites · 2026Article
- Targeting mitochondrial oxidative stress: A novel therapeutic strategy for degenerative joint diseases (Review).Biomedical reports · 2026Review
- Molecular characterization of Kawasaki disease subgroups using cell-free RNA profiling.Scientific reports · 2025Article
- Nuclear PKM2: a signal receiver, a gene programmer, and a metabolic modulator.Journal of biomedical science · 2025Review
- Phytochemical modulation of mTOR signaling: emerging nanotechnology-driven therapeutics for rheumatoid arthritis management.Inflammopharmacology · 2025Review
- The Role of PKM2 in Multiple Signaling Pathways Related to Neurological Diseases.Molecular neurobiology · 2024Review
- Targeting TLR Signaling Cascades in Systemic Lupus Erythematosus and Rheumatoid Arthritis: An Update.Biomedicines · 2024Article
- Targeting glycolytic pathway in fibroblast-like synoviocytes for rheumatoid arthritis therapy: challenges and opportunities.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Glucocorticoid receptors involved in ginsenoside compound K ameliorate adjuvant arthritis by inhibiting the glycolysis of fibroblast-like synoviocytes via the NF-κB/HIF-1α pathway.Pharmaceutical biology · 2023Article
- An Update on Toll-like Receptor 2, Its Function and Dimerization in Pro- and Anti-Inflammatory Processes.International journal of molecular sciences · 2023Review
- Bacterial Lipoproteins Shift Cellular Metabolism to Glycolysis in Macrophages Causing Bone Erosion.Microbiology spectrum · 2023Article
- Norbergenin prevents LPS-induced inflammatory responses in macrophages through inhibiting NFκB, MAPK and STAT3 activation and blocking metabolic reprogramming.Frontiers in immunology · 2023Article
- The mammalian target of rapamycin contributes to synovial fibroblast pathogenicity in rheumatoid arthritis.Frontiers in medicine · 2023Article
- Cellular metabolic adaptations in rheumatoid arthritis and their therapeutic implications.Nature reviews. Rheumatology · 2022Review
- Mitochondrial Dysfunction and Oxidative Stress in Rheumatoid Arthritis.Antioxidants (Basel, Switzerland) · 2022Review
- Metabolites as drivers and targets in rheumatoid arthritis.Clinical and experimental immunology · 2022Article
- Extracellular pyruvate kinase M2 promotes osteoclastogenesis and is associated with radiographic progression in early rheumatoid arthritis.Scientific reports · 2022Article
- Assessment of disease activity in patients with rheumatoid arthritis using plasma tumour M2-pyruvate kinase test.Frontiers in immunology · 2022Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During inflammation, immune cells activated by toll-like receptors (TLRs) have the ability to undergo a bioenergetic switch towards glycolysis in a manner similar to that observed in tumour cells. While TLRs have been implicated in the pathogenesis of rheumatoid arthritis (RA), their role in regulating cellular metabolism in synovial cells, however, is still unknown. In this study, we investigated the effect of TLR2-activation on mitochondrial function and bioenergetics in primary RA-synovial fibroblast cells (RASFC), and further determined the role of glycolytic blockade on TLR2-induced inflammation in RASFC using glycolytic inhibitor 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one (3PO). We observed an increase in mitochondrial mutations, ROS and lipid peroxidation, paralleled by a decrease in the mitochondrial membrane potential in TLR2-stimulated RASFC. This was mirrored by differential regulation of key mitochondrial genes, coupled with alteration in mitochondrial morphology. TLR2-activation also regulated changes in the bioenergetic profile of RASFC, inducing PKM2 nuclear translocation, decreased mitochondrial respiration and ATP synthesis and increased glycolysis:respiration ratio, suggesting a metabolic switch. Finally, using 3PO, we demonstrated that glycolytic blockade reversed TLR2-induced pro-inflammatory mechanisms including invasion, migration, cytokine/chemokine secretion and signalling pathways. These findings support the concept of complex interplay between innate immunity, oxidative damage and oxygen metabolism in RA pathogenesis.
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