ArticleFrontiers in immunology2018
Kruppel-Like Factor 4 Positively Regulates Autoimmune Arthritis in Mouse Models and Rheumatoid Arthritis in Patients
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Integrating transcriptomic analysis to explore biomarkers and therapeutic targets for rheumatoid arthritis: a case-control and systems biology approach.Frontiers in bioinformatics · 2026Article
- Progress and prospect of minicircle as a minimized non-viral DNA vector in gene therapy and regenerative medicine.Molecular therapy. Nucleic acids · 2025Review
- Circular RNA Cdr1as Modulates Macrophage-Mediated Cardiac Reparative Function.Circulation research · 2025Article
- KLF11 alleviates rheumatoid arthritis by regulating M1 macrophage polarization via downregulation of YAP1 expression.Arthritis research & therapy · 2025Article
- Exosomal miR-146a-5p Derived from HSCs Accelerates Sepsis-induced Liver Injury by Suppressing KLF-4.Inflammation · 2025Article
- Expression of miR-92a in Green Tea EGCG Preconditioned Adiposederived Stem Cells Ameliorates Inflammatory Response and Increases Cartilage Regeneration in RA Rats through KLF4/IL-17/MMP-2 Axis Modulation.Current gene therapy · 2025Article
- Krüppel-like factors in mitochondrial quality control.Frontiers in physiology · 2025Review
- The KLF4/Galectin-3 cascade is a key determinant of tubular cell death and acute kidney injury.International journal of biological sciences · 2025Article
- KLF transcription factors in bone diseases.Journal of cellular and molecular medicine · 2024Review
- α-parvin controls chondrocyte column formation and regulates long bone development.Bone research · 2023Article
- Cellular and Molecular Targets of Extracellular Vesicles from Mesenchymal Stem/Stromal Cells in Rheumatoid Arthritis.Stem cells translational medicine · 2022Review
- Inhibition of Kruppel-like factor 7 attenuates cell proliferation and inflammation of fibroblast-like synoviocytes in rheumatoid arthritis through nuclear factor κB and mitogen-activated protein kinase signaling pathway.Experimental animals · 2022Article
- KLF4 downregulates FGF21 to activate inflammatory injury and oxidative stress of LPS‑induced ATDC5 cells via SIRT1/NF‑κB/p53 signaling.Molecular medicine reports · 2022Article
- Minicircles for Investigating and Treating Arthritic Diseases.Pharmaceutics · 2021Review
- Network analysis indicating the pharmacological mechanism of Yunpi-Qufeng-Chushi-prescription in prophylactic treatment of rheumatoid arthritis.BMC complementary medicine and therapies · 2021Article
- MicroRNA-21 from bone marrow mesenchymal stem cell-derived extracellular vesicles targets TET1 to suppress KLF4 and alleviate rheumatoid arthritis.Therapeutic advances in chronic disease · 2021Article
- Modulation of IL-6 Expression by KLF4-Mediated Transactivation and PCAF-Mediated Acetylation in Sublytic C5b-9-Induced Rat Glomerular Mesangial Cells.Frontiers in immunology · 2021Article
- Improving therapeutic potential of non-viral minimized DNA vectors.Cell & gene therapy insights · 2020Article
- Yeast Cell wall Particle mediated Nanotube-RNA delivery system loaded with miR365 Antagomir for Post-traumatic Osteoarthritis Therapy via Oral Route.Theranostics · 2020Article
- Integrative Approach to Reveal Cell Type Specificity and Gene Candidates for Psoriatic Arthritis Outside the MHC.Frontiers in genetics · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) is a chronic autoimmune disease that causes mild to severe joint inflammation. During RA pathogenesis, fibroblast-like synoviocytes (FLS) acquire a tumor-like phenotype and mediate cartilage destruction both directly and indirectly by producing proinflammatory cytokines and matrix metalloproteinases (MMPs). Kruppel-like factor (KLF) 4, a member of the KLF family, plays significant roles in cell survival, proliferation, and differentiation. A recent study reported increased expression of KLF4 in synovial tissue from RA patients. However, its precise role in RA in different models, including mouse autoimmune disease models, remains unclear. In this study, we examined the role of KLF4 during development of autoimmune arthritis in mouse models. To do this, we used KLF4 knockout mice rendered by ribonucleic acid (RNA)-guided endonuclease (RGEN) and performed collagen antibody-induced arthritis (CAIA). We found that deletion of KLF4 reduces inflammation induced by CAIA. In addition, we assessed collagen-induced arthritis (CIA) in control mice and KLF4-overexpressing mice generated by a minicircle vector treatment. Severity of CIA in mice overexpressing KLF4 was greater than that in mice injected with control vector. Finally, we verified the inflammatory roles of KLF4 in CIA by treating Kenpaullone which is used as KLF4 inhibitor. Next, we focused on human/mouse FLS to discover the cellular process involved in RA pathogenesis including proliferation, apoptosis, and inflammation including MMPs. In FLS, KLF4 upregulated expression of mRNA encoding proinflammatory cytokines interleukin (IL)-1β and IL-6. KLF4 also regulated expression of matrix metallopeptidase 13 in the synovium. We found that blockade of KLF4 in FLS increased apoptosis and suppressed proliferation followed by downregulation of antiapoptotic factor BCL2. Our results indicate that KLF4 plays a crucial role in pathogenesis of inflammatory arthritis
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