ReviewEBioMedicine2019
Krϋppel-like factors (KLFs) in renal physiology and disease.
Review in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
104 citing papers in PubMed, 184 citations in OpenAlex.
- Glis3 Is a Modifier of Cyst Progression in Autosomal Dominant Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2026Article
- Kidney organoid vascularization: current advancements in the field.Regenerative therapy · 2026Article
- Single-nucleus transcriptomics illuminates sex differences during murine Escherichia coli pyelonephritis.Communications biology · 2026Article
- TGF-β1/SMAD signaling downregulates KLF4 expression via direct transcriptional suppression and FAT10-mediated proteasomal degradation in hepatocellular carcinoma.Cell & bioscience · 2026Article
- The key role and research progress of endothelial cells in renal microcirculation.Frontiers in medicine · 2026Review
- Immune Infiltration-Related Genes as Potential Biomarkers and Predicted Targets for Renal Allograft Delayed Graft Function and Survival Outcome: An Integrated Machine Learning Approach and Drugs Analysis.Mediators of inflammation · 2026Article
- Macrophage Nrf1/NFE2L1-Foxo1 axis controls liver fibrosis by modulation of mitochondrial reprogramming.Theranostics · 2026Article
- Targeting CDC42 Protects Mitochondrial Function through KLF2/HIF-1α/PINK1 Signaling in Acute Kidney Injury.International journal of biological sciences · 2026Article
- Decoding the Kruppel-like Transcription Factors in Atherosclerosis: Insight from Molecular and Translational Perspectives.International journal of molecular sciences · 2025Review
- Cholangiocyte-derived exosomal miR-381-3p promotes hepatic stellate cell activation and cholestatic liver fibrosis via targeting Klf6.Regenerative therapy · 2025Article
- Review
- Mechanical Stress and Protective Mechanisms in Podocytes: Insights into Hypertensive Nephropathy.International journal of molecular sciences · 2025Review
- ODC1 loss upon KLF6 upregulation promotes macrophage pyroptosis and acute kidney injury in sepsis.Human cell · 2025Article
- Ferroptosis in Cancer and Inflammatory Diseases: Mechanisms and Therapeutic Implications.MedComm · 2025Review
- Basophil-derived exosomes exacerbate systemic lupus erythematosus by regulating B-cell proliferation via miR-24550.BMC medicine · 2025Article
- Apelin/APJ alleviates diabetic nephropathy by improving glomerular endothelial cells dysfunction via SIRT3‑KLF15.Molecular medicine reports · 2025Article
- EPB41L3 Inhibits the Progression of Cervical Cancer Via the ERK/p38 MAPK Signaling Pathway.Molecular biotechnology · 2025Article
- The integrin repertoire drives YAP-dependent epithelial:stromal interactions during injury of the kidney glomerulus.Nature communications · 2025Article
- High Glucose Treatment Induces Nuclei Aggregation of Microvascular Endothelial Cells via theArteriosclerosis, thrombosis, and vascular biology · 2025Article
- METTL10 attenuates adriamycin-induced podocyte injury by targeting cell dedifferentiation.Scientific reports · 2025Article
44 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulated Krϋppel-like factor (KLF) gene expression appears in many disease-associated pathologies. In this review, we discuss physiological functions of KLFs in the kidney with a focus on potential pharmacological modulation/therapeutic applications of these KLF proteins. KLF2 is critical to maintaining endothelial barrier integrity and preventing gap formations and in prevention of glomerular endothelial cell and podocyte damage in diabetic mice. KLF4 is renoprotective in the setting of AKI and is a critical regulator of proteinuria in mice and humans. KLF6 expression in podocytes preserves mitochondrial function and prevents podocyte apoptosis, while KLF5 expression prevents podocyte apoptosis by blockade of ERK/p38 MAPK pathways. KLF15 is a critical regulator of podocyte differentiation and is protective against podocyte injury. Loss of KLF4 and KLF15 promotes renal fibrosis, while fibrotic kidneys have increased KLF5 and KLF6 expression. For therapeutic modulation of KLFs, continued screening of small molecules will promote drug discoveries targeting KLF proteins.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.