ArticleExperimental animals2022
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.
Article in Experimental animals, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- MLL1-pioneered H3K4me3 modification on KLF7 promoter accelerates the invasion of fibroblast-like synoviocytes in rheumatoid arthritis.In vitro cellular & developmental biology. Animal · 2026Article
- Remarkable heterogeneity revealed in the genetic architecture of resistance to a key bacterial pathogen in two commercial rainbow trout populations.BMC genomics · 2025Article
- KLF11 alleviates rheumatoid arthritis by regulating M1 macrophage polarization via downregulation of YAP1 expression.Arthritis research & therapy · 2025Article
- Zinc fingers are responsible for the efficient control of KLF7 on the transcription of genes in the NF-κB signaling pathway and fatty acid β-oxidation.Acta biochimica et biophysica Sinica · 2025Article
- KLF7 enhances the inflammatory response in LPS-induced alveolar epithelial cellsCentral-European journal of immunology · 2025Article
- Single-cell analysis reveals the loss of FABP4-positive proliferating valvular endothelial cells relates to functional mitral regurgitation.BMC medicine · 2024Article
- KLF transcription factors in bone diseases.Journal of cellular and molecular medicine · 2024Review
- Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) is an autoimmune disease, which can lead to joint inflammation and progressive joint destruction. Kruppel-like factor 7 (KLF7) is the member of KLF family and plays an important role in multiple biological progresses. However, its precise roles in RA have not been described. Present study aimed to investigate the role of KLF7 in RA-fibroblast-like synoviocytes (FLSs). Data showed that KLF7 expression was obviously upregulated in synovial tissues of rats with adjuvant-induced arthritis. Functional studies demonstrated that the loss of KLF7 may suppress cell proliferation and the expression of pro-inflammatory factors (IL-6, IL-1β, IL-17A) and matrix metalloproteinase (MMP-1, MMP-3, MMP-13) in FLSs through the inhibition of phosphorylation of nuclear factor κB (NF-κB) p65 and JNK. We further showed that miR-9a-5p specifically interacts with KLF7 to negatively regulate the expression of KLF7 in RA-FLSs. Taken together, our results demonstrated that KLF7 which targeted by miR-9a-5p might participate in the pathogenesis of RA by promoting cell proliferation, pro-inflammatory cytokine release and MMP expression through the activation of NF-κB and JNK pathways in RA-FLSs. Hence, KLF7 could be a novel target for RA therapy.
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