ArticlePloS one2022
KLF11 deficiency enhances chemokine generation and fibrosis in murine unilateral ureteral obstruction.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Stem cell activation in organ culture reveals novel transcriptional programs underlying metabolic, fibrotic, vascular, and immune dysregulation in uterine leiomyomas.Frontiers in cell and developmental biology · 2026Article
- KLF11 alleviates rheumatoid arthritis by regulating M1 macrophage polarization via downregulation of YAP1 expression.Arthritis research & therapy · 2025Article
- Exploring the Functionality of the Krüppel-like Factors in Kidney Development, Metabolism, and Diseases.Life (Basel, Switzerland) · 2024Review
- Endothelial KLF11 is a novel protector against diabetic atherosclerosis.Cardiovascular diabetology · 2024Article
- [Upregulating KLF11 ameliorates intestinal inflammation in mice with 2, 4, 6-trinitrobenesulfonic acid-induced colitis by inhibiting the JAK2/STAT3 signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- An integrated co-expression network analysis reveals novel genetic biomarkers for immune cell infiltration in chronic kidney disease.Frontiers in immunology · 2023Article
- Endothelial KLF11 as a Nephroprotectant in AKI.Kidney360 · 2022Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progression of virtually all forms of chronic kidney disease (CKD) is associated with activation of pro-inflammatory and pro-fibrotic signaling pathways. Despite extensive research, progress in identifying therapeutic targets to arrest or slow progression of CKD has been limited by incomplete understanding of basic mechanisms underlying renal inflammation and fibrosis in CKD. Recent studies have identified Kruppel-like transcription factors that have been shown to play critical roles in renal development, homeostasis, and response to injury. Although KLF11 deficiency has been shown to increase collagen production in vitro and tissue fibrosis in other organs, no previous study has linked KLF11 to the development of CKD. We sought to test the hypothesis that KLF11 deficiency promotes CKD through upregulation of pro-inflammatory and pro-fibrogenic signaling pathways in murine unilateral ureteral obstruction (UUO), a well-established model of renal fibrosis. We found that KLF11-deficiency exacerbates renal injury in the UUO model through activation of the TGF-β/SMAD signaling pathway and through activation of several pro-inflammatory chemokine signaling pathways. Based on these considerations, we conclude that agents increase KLF11 expression may provide novel therapeutic targets to slow the progression of CKD.
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Registered trials
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