ArticleScience advances2021
Podocyte-specific KLF4 is required to maintain parietal epithelial cell quiescence in the kidney.
Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 32 citations in OpenAlex.
- Functional characterization of podocyte-expressed THSD7A in experimental membranous nephropathy.JCI insight · 2026Article
- Application of the nephrotoxic serum nephritis model in glomerulonephritis research.Molecular medicine (Cambridge, Mass.) · 2026Review
- miR-135a-5p Is a Promising Target to Prevent the Glomerulosclerosis Associated with Podocyte Developmental Toxicity in Offspring Induced by Prenatal Dexamethasone Exposure.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Signal Transducer and Activator of Transcription 3 in the Podocyte: A Key Mediator of Podocyte-Parietal Epithelial Cell Cross-Talk and Glomerular Health?Journal of the American Society of Nephrology : JASN · 2026Article
- Podocyte-Specific Deletion of STAT3 in Krüppel-Like Factor 4-Related Experimental Podocytopathy.Journal of the American Society of Nephrology : JASN · 2026Article
- Article
- Krüppel-Like Factor 6 Induces RNA Polymerase II Subunit RPB1 to Promote Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Article
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- Podocyte YAP and TAZ hyperactivation drives glomerular epithelial proliferative diseases in mice and humans.Science translational medicine · 2025Article
- Piezo1, F-Actin Remodeling, and Podocyte Survival and Regeneration.Journal of the American Society of Nephrology : JASN · 2025Article
- Article
- The KLF4/Galectin-3 cascade is a key determinant of tubular cell death and acute kidney injury.International journal of biological sciences · 2025Article
- Podocyte-specific KLF6 primes proximal tubule CaMK1D signaling to attenuate diabetic kidney disease.Nature communications · 2024Article
- Central role of podocytes in mediating cellular cross talk in glomerular health and disease.American journal of physiology. Renal physiology · 2024Review
- Podocyte-specific Transcription Factors: Could MafB Become a Therapeutic Target for Kidney Disease?Internal medicine (Tokyo, Japan) · 2023Review
- Heterozygous expression of Cre recombinase in podocytes has no impact on the anti-glomerular basement membrane glomerulonephritis model in C57BL/6J mice.Physiological reports · 2022Article
- Signaling pathways of chronic kidney diseases, implications for therapeutics.Signal transduction and targeted therapy · 2022Review
- Altered DNA methylation in kidney disease: useful markers and therapeutic targets.Clinical and experimental nephrology · 2022Review
- The Role of Parietal Epithelial Cells in the Pathogenesis of Podocytopathy.Frontiers in physiology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
Podocyte loss triggering aberrant activation and proliferation of parietal epithelial cells (PECs) is a central pathogenic event in proliferative glomerulopathies. Podocyte-specific Krüppel-like factor 4 (KLF4), a zinc-finger transcription factor, is essential for maintaining podocyte homeostasis and PEC quiescence. Using mice with podocyte-specific knockdown of Klf4, we conducted glomerular RNA-sequencing, tandem mass spectrometry, and single-nucleus RNA-sequencing to identify cell-specific transcriptional changes that trigger PEC activation due to podocyte loss. Integration with in silico chromatin immunoprecipitation identified key ligand-receptor interactions, such as fibronectin 1 (FN1)–αVβ6, between podocytes and PECs dependent on KLF4 and downstream signal transducer and activator of transcription 3 (STAT3) signaling. Knockdown of Itgb6 in PECs attenuated PEC activation. Additionally, podocyte-specific induction of human KLF4 or pharmacological inhibition of downstream STAT3 activation reduced FN1 and integrin β 6 (ITGB6) expression and mitigated podocyte loss and PEC activation in mice. Targeting podocyte-PEC crosstalk might be a critical therapeutic strategy in proliferative glomerulopathies.
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.