ArticleThe Journal of biological chemistry2012
Kruppel-like factor 15 (KLF15) is a key regulator of podocyte differentiation.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 102 citations in OpenAlex.
- The CaPediatric nephrology (Berlin, Germany) · 2025Review
- Inhibition of epigenetic regulator UHRF1 attenuates renal fibrosis and retains transcription factor Krüppel-like factor 15 expression.Cell death discovery · 2025Article
- Cell cycle disorders in podocytes: an emerging and increasingly recognized phenomenon.Cell death discovery · 2025Review
- Effects of Graphene Quantum Dots on Renal Fibrosis Through Alleviating Oxidative Stress and Restoring Mitochondrial Membrane Potential.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Protecting Podocytes in Glomerular Diseases Beyond Glucocorticoids.Journal of the American Society of Nephrology : JASN · 2024Article
- A Small Molecule Agonist of Krüppel-Like Factor 15 in Proteinuric Kidney Disease.Journal of the American Society of Nephrology : JASN · 2024Article
- Podocyte-targeted therapies - progress and future directions.Nature reviews. Nephrology · 2024Review
- Targeting microRNA-190a halts the persistent myofibroblast activation and oxidative stress accumulation through upregulation of Krüppel-like factor 15 in oral submucous fibrosis.Journal of dental sciences · 2024Article
- Podocyte-specific KLF6 primes proximal tubule CaMK1D signaling to attenuate diabetic kidney disease.Nature communications · 2024Article
- Article
- Crosstalk among podocytes, glomerular endothelial cells and mesangial cells in diabetic kidney disease: an updated review.Cell communication and signaling : CCS · 2024Review
- Metabolic adaptations in pressure overload hypertrophic heart.Heart failure reviews · 2024Review
- The transcriptional regulator KLF15 is necessary for myoblast differentiation and muscle regeneration by activating FKBP5.The Journal of biological chemistry · 2023Article
- TYRO3 agonist as therapy for glomerular disease.JCI insight · 2023Article
- Drosophila melanogaster: a simple genetic model of kidney structure, function and disease.Nature reviews. Nephrology · 2022Review
- How immunosuppressive drugs may directly target podocytes in glomerular diseases.Pediatric nephrology (Berlin, Germany) · 2022Review
- Article
- Renoprotective Effect of KLF2 on Glomerular Endothelial Dysfunction in Hypertensive Nephropathy.Cells · 2022Article
- Loss of proximal tubular transcription factor Krüppel-like factor 15 exacerbates kidney injury through loss of fatty acid oxidation.Kidney international · 2021Article
- Recent Advances in Diabetic Kidney Diseases: From Kidney Injury to Kidney Fibrosis.International journal of molecular sciences · 2021Review
9 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
Abstract
Podocyte injury resulting from a loss of differentiation is the hallmark of many glomerular diseases. We previously showed that retinoic acid (RA) induces podocyte differentiation via stimulation of the cAMP pathway. However, many podocyte maturity markers lack binding sites for RA-response element or cAMP-response element (CREB) in their promoter regions. We hypothesized that transcription factors induced by RA and downstream of CREB mediate podocyte differentiation. We performed microarray gene expression studies in human podocytes treated with and without RA to identify differentially regulated genes. In comparison with known CREB target genes, we identified Krüppel-like factor 15 (KLF15), a kidney-enriched nuclear transcription factor, that has been previously shown to mediate cell differentiation. We confirmed that RA increased KLF15 expression in both murine and human podocytes. Overexpression of KLF15 stimulated expression of differentiation markers in both wild-type and HIV-1-infected podocytes. Also, KLF15 binding to the promoter regions of nephrin and podocin was increased in RA-treated podocytes. Although KLF15(-/-) mice at base line had minimal phenotype, lipopolysaccharide- or adriamycin-treated KLF15(-/-) mice had a significant increase in proteinuria and podocyte foot process effacement with a reduction in the expression of podocyte differentiation markers as compared with the wild-type treated mice. Finally, KLF15 expression was reduced in glomeruli isolated from HIV transgenic mice as well as in kidney biopsies from patients with HIV-associated nephropathy and idiopathic focal segmental glomerulosclerosis. These results indicate a critical role of KLF15 in mediating podocyte differentiation and in protecting podocytes against injury.
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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 OpenQuestion graph.