ArticleAmerican journal of physiology. Renal physiology2010
Dose- and time-dependent glucocorticoid receptor signaling in podocytes.
Article in American journal of physiology. Renal physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.
What it found
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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
44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 65 citations in OpenAlex.
- Corticosteroid therapy for nephrotic syndrome in children.The Cochrane database of systematic reviews · 2024Pooled it
- Corticosteroid therapy for nephrotic syndrome in children.The Cochrane database of systematic reviews · 2020Pooled it
- Open-Label Clinical Trials of Oral Pulse Dexamethasone for Adults with Idiopathic Nephrotic Syndrome.American journal of nephrology · 2019Trial
- Review
- The CaPediatric nephrology (Berlin, Germany) · 2025Review
- Effects of Prothrombin on Podocytopathy and Proteinuria in Glomerular Disease.Journal of the American Society of Nephrology : JASN · 2025Article
- A Small Molecule Agonist of Krüppel-Like Factor 15 in Proteinuric Kidney Disease.Journal of the American Society of Nephrology : JASN · 2024Article
- Inhibition of the glucocorticoid receptor attenuates proteinuric kidney diseases in multiple species.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024Article
- Podocyte number and glomerulosclerosis indices are associated with the response to therapy for primary focal segmental glomerulosclerosis.Frontiers in medicine · 2024Article
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- TYRO3 agonist as therapy for glomerular disease.JCI insight · 2023Article
- Steroid Minimization in Adults with Minimal Change Disease.Glomerular diseases · 2021Review
- Review
- Regulation of Melanophilin (Mlph) gene expression by the glucocorticoid receptor (GR).Scientific reports · 2021Article
- Podocyte Glucocorticoid Receptors Are Essential for Glomerular Endothelial Cell Homeostasis in Diabetes Mellitus.Journal of the American Heart Association · 2021Article
- Nuclear receptors in podocyte biology and glomerular disease.Nature reviews. Nephrology · 2021Review
- Review
- Unraveling the Role of Inflammation in the Pathogenesis of Diabetic Kidney Disease.International journal of molecular sciences · 2019Review
- Role of the glucocorticoid receptor in glomerular disease.American journal of physiology. Renal physiology · 2019Review
- Pharmacology and pharmacogenetics of prednisone and prednisolone in patients with nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Glucocorticoids (GC) are the primary therapy for idiopathic nephrotic syndrome (NS). Recent evidence has identified glomerular podocytes as a potential site of GC action in this disease. The objectives of this study were to determine the presence of key components of the glucocorticoid receptor (GR) complex and the functionality of this signaling pathway in podocytes and to explore potential opportunities for manipulation of GC responsiveness. Here, we show that cultured murine podocytes express key components of the GR complex, including the GR, heat shock protein 90, and the immunophilins FKBP51 and FKBP52. The functionality of GR-mediated signaling was verified by measuring several GC (dexamethasone)-induced responses, including 1) increases in mRNA and protein levels of selected GC-regulated genes (FKBP51, phenol sulfotransferase 1, αB-crystallin); 2) downregulation of the GR protein; 3) increased phosphorylation of the GR; and 4) translocation of the GR into the nuclear fraction. Dexamethasone-induced phosphorylation and downregulation of GR protein were also demonstrated in isolated rat glomeruli. Podocyte gene expression in response to dexamethasone was regulated at both the transcriptional and posttranscriptional levels, the latter also including protein degradation. Short-term, high-dose GC treatment resulted in similar changes in gene expression and GR phosphorylation to that of long-term, low-dose GC treatment, thus providing a molecular rationale for the known efficacy of pulse GC therapy in NS. Induction of FKBP51 and downregulation of the GR represent negative feedback mechanisms that can potentially be exploited to improve clinical GC efficacy. Collectively, these findings demonstrate the presence of key molecular components of the GR signaling pathway and its functionality in podocytes and identify novel opportunities for improving clinical GC efficacy in the treatment of NS.
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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 OpenQuestion graph.