ArticleScientific reports2017
Glucocorticoid therapy regulates podocyte motility by inhibition of Rac1.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- Mechanisms of Podocyte Injury in Kidney Allografts.Kidney360 · 2026Review
- Review
- The CaPediatric nephrology (Berlin, Germany) · 2025Review
- Extracellular Vesicle Mitochondrial DNA Reflects Podocyte Mitochondrial Stress and Is Associated with Relapse in Nephrotic Syndrome.International journal of molecular sciences · 2025Article
- Podocytes in health and glomerular disease.Frontiers in cell and developmental biology · 2025Review
- Circulating RAC1 contributed to steroid-sensitive nephrotic syndrome: Mendelian randomization, single-cell RNA-sequencing, proteomic, and experimental evidence.Renal failure · 2024Article
- Podocyte-targeted therapies - progress and future directions.Nature reviews. Nephrology · 2024Review
- Cytoskeleton Rearrangement in Podocytopathies: An Update.International journal of molecular sciences · 2024Review
- How immunosuppressive drugs may directly target podocytes in glomerular diseases.Pediatric nephrology (Berlin, Germany) · 2022Review
- New Insights into the Treatment of Glomerular Diseases: When Mechanisms Become Vivid.International journal of molecular sciences · 2022Review
- Glomerulus-on-a-Chip: Current Insights and Future Potential Towards Recapitulating Selectively Permeable Filtration Systems.International journal of nephrology and renovascular disease · 2022Review
- Rho GTPases in kidney physiology and diseases.Small GTPases · 2022Article
- Glucocorticoid receptor wields chromatin interactions to tune transcription for cytoskeleton stabilization in podocytes.Communications biology · 2021Article
- Glucocorticoids rapidly inhibit cell migration through a novel, non-transcriptional HDAC6 pathway.Journal of cell science · 2020Article
- Role of the glucocorticoid receptor in glomerular disease.American journal of physiology. Renal physiology · 2019Review
- FHL2 mediates podocyte Rac1 activation and foot process effacement in hypertensive nephropathy.Scientific reports · 2019Article
- Genetic variants in the LAMA5 gene in pediatric nephrotic syndrome.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2019Article
- Podocyte RhoGTPases: new therapeutic targets for nephrotic syndrome?F1000Research · 2019Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
Abstract
Nephrotic syndrome (NS) occurs when the glomerular filtration barrier becomes excessively permeable leading to massive proteinuria. In childhood NS, immune system dysregulation has been implicated and increasing evidence points to the central role of podocytes in the pathogenesis. Children with NS are typically treated with an empiric course of glucocorticoid (Gc) therapy; a class of steroids that are activating ligands for the glucocorticoid receptor (GR) transcription factor. Although Gc-therapy has been the cornerstone of NS management for decades, the mechanism of action, and target cell, remain poorly understood. We tested the hypothesis that Gc acts directly on the podocyte to produce clinically useful effects without involvement of the immune system. In human podocytes, we demonstrated that the basic GR-signalling mechanism is intact and that Gc induced an increase in podocyte barrier function. Defining the GR-cistrome identified Gc regulation of motility genes. These findings were functionally validated with live-cell imaging. We demonstrated that treatment with Gc reduced the activity of the pro-migratory small GTPase regulator Rac1. Furthermore, Rac1 inhibition had a direct, protective effect on podocyte barrier function. Our studies reveal a new mechanism for Gc action directly on the podocyte, with translational relevance to designing new selective synthetic Gc molecules.
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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.