ArticleKidney international2015
The phenotypes of podocytes and parietal epithelial cells may overlap in diabetic nephropathy.
Article in Kidney international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 69 citations in OpenAlex.
- FGF4-FGFR1 signaling promotes podocyte survival and glomerular function to ameliorate diabetic kidney disease in male mice.Nature communications · 2025Article
- Continuous increase in podocyte numbers in the first 36 months of life-insights from forensic autopsies in Japanese children.Pediatric nephrology (Berlin, Germany) · 2025Article
- Review
- Preclinical Detection of Early Glomerular Injury in Children with Kidney Diseases-Independently of Usual Markers of Kidney Impairment and Inflammation.International journal of molecular sciences · 2024Article
- Mice with aAmerican journal of physiology. Renal physiology · 2024Article
- Dock5 Deficiency Promotes Proteinuric Kidney Diseases via Modulating Podocyte Lipid Metabolism.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Podocyte number and glomerulosclerosis indices are associated with the response to therapy for primary focal segmental glomerulosclerosis.Frontiers in medicine · 2024Article
- Review
- Diabetic nephropathy with marked extra-capillary cell proliferation: a case report.BMC nephrology · 2023Article
- Sestrin2 Signaling Pathway Regulates Podocyte Biology and Protects against Diabetic Nephropathy.Journal of diabetes research · 2023Review
- Mechanisms of podocyte injury and implications for diabetic nephropathy.Clinical science (London, England : 1979) · 2022Article
- Molecular Mechanisms of Kidney Injury and Repair.International journal of molecular sciences · 2022Review
- Cellular phenotypic transitions in diabetic nephropathy: An update.Frontiers in pharmacology · 2022Review
- The Role of Parietal Epithelial Cells in the Pathogenesis of Podocytopathy.Frontiers in physiology · 2022Review
- Renal cell markers: lighthouses for managing renal diseases.American journal of physiology. Renal physiology · 2021Article
- The recruitment mechanisms and potential therapeutic targets of podocytes from parietal epithelial cells.Journal of translational medicine · 2021Review
- Parietal epithelial cell dysfunction in crescentic glomerulonephritis.Cell and tissue research · 2021Review
- Combined Melatonin and Extracorporeal Shock Wave Therapy Enhances Podocyte Protection and Ameliorates Kidney Function in a Diabetic Nephropathy Rat Model.Antioxidants (Basel, Switzerland) · 2021Article
- Growth hormone induces mitotic catastrophe of glomerular podocytes and contributes to proteinuria.Cell death & disease · 2021Article
- Diabetic condition induces hypertrophy and vacuolization in glomerular parietal epithelial cells.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Reversal of diabetic nephropathy (DN) has been achieved in humans and mice, but only rarely and under special circumstances. As progression of DN is related to podocyte loss, reversal of DN requires restoration of podocytes. Here, we identified and quantified potential glomerular progenitor cells that could be a source for restored podocytes. DN was identified in 31 human renal biopsy cases and separated into morphologically early or advanced lesions. Markers of podocytes (WT-1, p57), parietal epithelial cells (PECs) (claudin-1), and cell proliferation (Ki-67) were identified by immunohistochemistry. Podocyte density was progressively reduced with DN. Cells marking as podocytes (p57) were present infrequently on Bowman's capsule in controls, but significantly increased in histologically early DN. Ki-67-expressing cells were identified on the glomerular tuft and Bowman's capsule in DN, but rarely in controls. Cells marking as PECs were present on the glomerular tuft, particularly in morphologically advanced DN. These findings show evidence of phenotypic plasticity in podocyte and PEC populations and are consistent with studies in the BTBR ob/ob murine model in which reversibility of DN occurs with podocytes potentially regenerating from PEC precursors. Thus, our findings support, but do not prove, that podocytes may regenerate from PEC progenitors in human DN. If so, progression of DN may represent a modifiable net balance between podocyte loss and regeneration.
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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.