ArticleExperimental & molecular medicine2025
mtSTAT3 suppresses rheumatoid arthritis by regulating Th17 and synovial fibroblast inflammatory cell death with IL-17-mediated autophagy dysfunction.
Article in Experimental & molecular medicine, 2025. 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.
- Natural Bioactive Compounds in Rheumatoid Arthritis: Experimental Evidence from Adjuvant Arthritis Model Supporting Combination Strategies with Methotrexate.International journal of molecular sciences · 2026Review
- Rheumatoid arthritis and airway hyperresponsiveness: A GWAS-based mendelian randomization study.Medicine · 2026Article
- Article
- Association of serum TNF-α, IL-17 A, and IL-17 F levels with disease activity in Yemeni patients with rheumatoid arthritis.Scientific reports · 2026Article
- Fraxin Attenuates Rheumatoid Arthritis by Regulating Macrophage Polarization and Inhibiting Fibroblast-like Synoviocyte Proliferation.International journal of molecular sciences · 2026Article
- Microbial metabolism of methotrexate produces a STAT3 signaling molecule that alleviates gut inflammation.bioRxiv : the preprint server for biology · 2026Article
- Dehydrocorydaline treatment suppresses Th17 differentiation via the mTOR-mediated STAT3-RORγt signaling in systemic lupus erythematosus.Molecular medicine (Cambridge, Mass.) · 2026Article
- NGO ameliorates psoriasis by modulating mitochondrial function and suppressing pSTAT3-IL-17-expressing CD8Journal of nanobiotechnology · 2026Article
- Osteoimmunology: interactions of the bone and immune system.Frontiers in immunology · 2026Review
- Targeting the Th17/Treg axis: from immunological insights to therapeutic avenues in atherosclerosis.Frontiers in immunology · 2026Review
- Estrogen and progesterone-mediated differential modulation of CD4Frontiers in immunology · 2026Article
- Emerging Insights into the Interplay Between PANoptosis and Autophagy in Immune Regulation and Immune-Mediated Inflammatory Diseases.Medical sciences (Basel, Switzerland) · 2025Review
- Multifunctional nanotherapeutics reprogramming the immunopathological landscape for rheumatoid arthritis therapy.Materials today. Bio · 2025Review
- Peptide ES15-1 derived from Haemonchus contortus promotes goat Th17 response by regulating the STAT3/RORγt pathway.Veterinary research · 2025Article
- Cardiac arrest triggers IL-17-mediated neuroinflammation and astrocyte polarization: insights into pathogenesis and intervention.Journal of neuroinflammation · 2025Article
- Preconditioning of bone marrow mesenchymal stem cells with sodium hydrosulfide enhances their therapeutic potential in type II collagen-induced arthritis rat model.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
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12 authors.
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Abstract
Th17 cells are activated by STAT3 factors in the nucleus, and these factors are correlated with the pathologic progression of rheumatoid arthritis (RA). Recent studies have demonstrated the presence of STAT3 in mitochondria, but its function is unclear. We investigated the novel role of mitochondrial STAT3 (mitoSTAT3) in Th17 cells and fibroblast-like synoviocytes (FLSs) and analyzed the correlation of mitoSTAT3 with RA. We used a collagen-induced arthritis (CIA) mouse model to determine the effect of mitochondrial STAT3. We observed changes in the RA mouse model via the use of a mitochondrial STAT3-inducing vector and inhibitor. We observed the accumulation of abnormal autophagosomes, increased inflammatory cell death signaling, and decreased mitoSTAT3 activity in FLSs from both patients with RA and patients with IL-17-treated FLSs. We first discovered that IL-17 increased the accumulation of abnormal autophagosomes and the expression of inflammatory cell death factors in synovial fibroblasts and decreased mitoSTAT3 activation. In a mouse model of CIA, arthritis and joint inflammation were decreased by injection vectors that induced mitoSTAT3 overexpression. The abnormal accumulation of autophagosomes and the expression of inflammatory cell death factors were also decreased in these mice. In mouse and human immune cells, ZnSO
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