ArticleAmerican journal of physiology. Renal physiology2013
Podocyte repopulation by renal progenitor cells following glucocorticoids treatment in experimental FSGS.
Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 109 citations in OpenAlex.
- Elovl7 sensitizes podocytes to ferroptosis in podocytopathy by elongating polyunsaturated fatty acids.Cell death & disease · 2025Article
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- Refining the adriamycin-induced focal segmental glomerulosclerosis mouse model to improve reproducibility and animal welfare.Animal models and experimental medicine · 2025Article
- Parietal epithelial cells in glomerulosclerosis: a new piece in the puzzle?Journal of nephrology · 2024Article
- Collapsing Glomerulopathy.Advances in kidney disease and health · 2024Review
- Podocyte number and glomerulosclerosis indices are associated with the response to therapy for primary focal segmental glomerulosclerosis.Frontiers in medicine · 2024Article
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- Upregulated PD-1 signaling antagonizes glomerular health in aged kidneys and disease.The Journal of clinical investigation · 2022Article
- Kidney injury and oxidative damage alleviation by3 Biotech · 2022Article
- Molecular Mechanisms of Kidney Injury and Repair.International journal of molecular sciences · 2022Review
- The Pathology Lesion Patterns of Podocytopathies: How and why?Frontiers in cell and developmental biology · 2022Review
- The Role of Parietal Epithelial Cells in the Pathogenesis of Podocytopathy.Frontiers in physiology · 2022Review
- The recruitment mechanisms and potential therapeutic targets of podocytes from parietal epithelial cells.Journal of translational medicine · 2021Review
- Steroid Minimization in Adults with Minimal Change Disease.Glomerular diseases · 2021Review
- Loss of phosphatidylserine flippase β-subunit Tmem30a in podocytes leads to albuminuria and glomerulosclerosis.Disease models & mechanisms · 2021Article
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- Nanoparticles exhibit greater accumulation in kidney glomeruli during experimental glomerular kidney disease.Physiological reports · 2020Article
- Repository corticotropin injection versus corticosteroids for protection against renal damage in a focal segmental glomerulosclerosis rodent model.BMC nephrology · 2020Article
- Renal progenitor cells modulated by angiotensin II receptor blocker (ARB) medication and differentiation towards podocytes in anti-thy1.1 nephritis.Annals of translational medicine · 2020Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Prednisone is a mainstay of treatment for patients with focal segmental glomerulosclerosis (FSGS), a disease characterized by reduced podocyte number and glomerulosclerosis. Although the systemic immune-modulatory effects of prednisone are well-known, direct tissue effects on glomerular cells are poorly understood. Experimental FSGS was induced in mice with a cytotoxic anti-podocyte antibody, resulting in an abrupt decrease in podocyte number by day 3, proteinuria, and the development of glomerulosclerosis. Administering daily prednisone to mice with FSGS, beginning at day 3, significantly increased podocyte number at weeks 2 and 4. Podocyte number did not increase in control mice with FSGS given DMSO. The increase in podocyte number in prednisone-treated mice correlated significantly with reduced glomerulosclerosis. Prednisone reduced podocyte apoptosis measured by synaptopodin⁺/caspase-3⁺ double staining. Additionally, the number of podocyte progenitors, defined as cells expressing both a parietal epithelial cell protein and a podocyte protein, was significantly increased in prednisone-treated mice with FSGS at weeks 2 and 4. This was associated with increased phospho-ERK staining in both parietal epithelial cells (PAX2⁺/p-ERK⁺) and in podocyte progenitors (WT-1⁺/p-ERK⁺ lining Bowman's capsule). These data show that in this model of experimental FSGS, prednisone augments glomerular repair by increasing podocyte number through direct effects on both glomerular epithelial cells. Prednisone limits podocyte loss by reducing apoptosis, and it increases regeneration by augmenting the number of podocyte progenitors. The data support a direct glomerular cell action for prednisone in improving outcomes in FSGS.
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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.