ArticleStem cell reports2015
Podocyte Regeneration Driven by Renal Progenitors Determines Glomerular Disease Remission and Can Be Pharmacologically Enhanced.
Article in Stem cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 136 citations in OpenAlex.
- Single-cell spatial mapping of human kidney development implicates the microenvironment in guiding cell fate decisions.Nature genetics · 2026Article
- Article
- Piezo1-Mediated Mechanotransduction: Orchestrating the Dynamic Response of Podocytes and Parietal Epithelial Cells to Mechanical Stress.Acta physiologica (Oxford, England) · 2026Review
- Decreased parietal epithelial cell density is linked to podocyte depletion and predictors of kidney disease progression in human kidneys.American journal of physiology. Renal physiology · 2025Article
- Mechanisms and Therapeutic Perspectives of Podocyte Aging in Podocytopathies.International journal of molecular sciences · 2025Review
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- Continuous increase in podocyte numbers in the first 36 months of life-insights from forensic autopsies in Japanese children.Pediatric nephrology (Berlin, Germany) · 2025Article
- Piezo1, F-Actin Remodeling, and Podocyte Survival and Regeneration.Journal of the American Society of Nephrology : JASN · 2025Article
- Mechanistic Insights Into Redox Damage of the Podocyte in Hypertension.Hypertension (Dallas, Tex. : 1979) · 2025Review
- Podocytes in health and glomerular disease.Frontiers in cell and developmental biology · 2025Review
- Sparsentan improves glomerular hemodynamics, cell functions, and tissue repair in a mouse model of FSGS.JCI insight · 2024Article
- Mice with aAmerican journal of physiology. Renal physiology · 2024Article
- (Zebra)fishing for nephrogenesis genes.Tissue barriers · 2024Review
- Central role of podocytes in mediating cellular cross talk in glomerular health and disease.American journal of physiology. Renal physiology · 2024Review
- Kidney lipid dysmetabolism and lipid droplet accumulation in chronic kidney disease.Nature reviews. Nephrology · 2023Review
- Preparation of Human Kidney Progenitor Cultures and Their Differentiation into Podocytes.Bio-protocol · 2023Article
- Inhibition of clonal expansion of parietal epithelial cells and crescent-podocyte transition in severe glomerulonephritis: on the way to targeted therapy?Clinical kidney journal · 2023Article
- Modeling Podocyte Ontogeny and Podocytopathies with the Zebrafish.Journal of developmental biology · 2023Review
- Parietal Epithelial Cell Behavior and Its Modulation by microRNA-193a.Biomolecules · 2023Review
- Defining diagnostic trajectories in patients with podocytopathies.Clinical kidney journal · 2022Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Podocyte loss is a general mechanism of glomerular dysfunction that initiates and drives the progression of chronic kidney disease, which affects 10% of the world population. Here, we evaluate whether the regenerative response to podocyte injury influences chronic kidney disease outcome. In models of focal segmental glomerulosclerosis performed in inducible transgenic mice where podocytes are tagged, remission or progression of disease was determined by the amount of regenerated podocytes. When the same model was established in inducible transgenic mice where renal progenitors are tagged, the disease remitted if renal progenitors successfully differentiated into podocytes, while it persisted if differentiation was ineffective, resulting in glomerulosclerosis. Treatment with BIO, a GSK3s inhibitor, significantly increased disease remission by enhancing renal progenitor sensitivity to the differentiation effect of endogenous retinoic acid. These results establish renal progenitors as critical determinants of glomerular disease outcome and a pharmacological enhancement of their differentiation as a possible therapeutic strategy.
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