ArticleScience translational medicine2022
Differentiation of crescent-forming kidney progenitor cells into podocytes attenuates severe glomerulonephritis in mice.
Article in Science translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Podocyte Metabolic Reprogramming and Targeted Therapy.Journal of the American Society of Nephrology : JASN · 2026Review
- Piezo1-Mediated Mechanotransduction: Orchestrating the Dynamic Response of Podocytes and Parietal Epithelial Cells to Mechanical Stress.Acta physiologica (Oxford, England) · 2026Review
- The Assessment of Disease Activity and Renal Prognosis in AAV - The Contribution of Urinary Biomarkers and Renal Biopsy.Current rheumatology reports · 2026Review
- Podocytopathies.Nature reviews. Disease primers · 2025Review
- Cellular senescence in kidney diseases.Chinese medical journal · 2025Review
- Podocyte YAP and TAZ hyperactivation drives glomerular epithelial proliferative diseases in mice and humans.Science translational medicine · 2025Article
- Kidney immunology from pathophysiology to clinical translation.Nature reviews. Immunology · 2025Review
- Piezo1, F-Actin Remodeling, and Podocyte Survival and Regeneration.Journal of the American Society of Nephrology : JASN · 2025Article
- Effects of reduced extracellular sodium on proliferation and invasive activity of renal cell carcinoma cell lines.Scientific reports · 2025Article
- Bowman's capsule rupture and its clinical significance in patients with anti-glomerular basement membrane disease.Frontiers in immunology · 2025Article
- Pathogenesis of HIV-associated nephropathy in children and adolescents: taking a hard look 40 years later in the era of gene-environment interactions.American journal of physiology. Renal physiology · 2024Review
- Review
- Course of paediatric ANCA-associated glomerulonephritis: advocating for an age-inclusive approach.RMD open · 2024Article
- Identification of mitophagy-related hub genes during the progression of spinal cord injury by integrated multinomial bioinformatics analysis.Biochemistry and biophysics reports · 2024Article
- Interferon and B-cell Signatures Inform Precision Medicine in Lupus Nephritis.Kidney international reports · 2024Article
- Role of biophysics and mechanobiology in podocyte physiology.Nature reviews. Nephrology · 2024Review
- Modeled microgravity unravels the roles of mechanical forces in renal progenitor cell physiology.Stem cell research & therapy · 2024Article
- Uncovering the Role of Anoikis-Related Genes in Modulating Immune Infiltration and Pathogenesis of Diabetic Kidney Disease.Journal of inflammation research · 2024Article
- Molecular characteristics of circulating B cells and kidney cells at the single-cell level in special types of primary membranous nephropathy.Clinical kidney journal · 2023Article
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Authors and funding
26 authors at 5 institutions in 3 countries.
Funding
Abstract
Crescentic glomerulonephritis is characterized by vascular necrosis and parietal epithelial cell hyperplasia in the space surrounding the glomerulus, resulting in the formation of crescents. Little is known about the molecular mechanisms driving this process. Inducing crescentic glomerulonephritis in two Pax2Cre reporter mouse models revealed that crescents derive from clonal expansion of single immature parietal epithelial cells. Preemptive and delayed histone deacetylase inhibition with panobinostat, a drug used to treat hematopoietic stem cell disorders, attenuated crescentic glomerulonephritis with recovery of kidney function in the two mouse models. Three-dimensional confocal microscopy and stimulated emission depletion superresolution imaging of mouse glomeruli showed that, in addition to exerting an anti-inflammatory and immunosuppressive effect, panobinostat induced differentiation of an immature hyperplastic parietal epithelial cell subset into podocytes, thereby restoring the glomerular filtration barrier. Single-cell RNA sequencing of human renal progenitor cells in vitro identified an immature stratifin-positive cell subset and revealed that expansion of this stratifin-expressing progenitor cell subset was associated with a poor outcome in human crescentic glomerulonephritis. Treatment of human parietal epithelial cells in vitro with panobinostat attenuated stratifin expression in renal progenitor cells, reduced their proliferation, and promoted their differentiation into podocytes. These results offer mechanistic insights into the formation of glomerular crescents and demonstrate that selective targeting of renal progenitor cells can attenuate crescent formation and the deterioration of kidney function in crescentic glomerulonephritis in mice.
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