ArticleJournal of the American Society of Nephrology : JASN2011
Podocyte injury damages other podocytes.
Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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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.
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Who cites it
66 citing papers in PubMed, 115 citations in OpenAlex.
- Urinary Podocyte Loss is Associated With Treatment Response in Patients With Primary Nephrotic Syndrome.Kidney international reports · 2026Article
- Biopsy Morphometrics as Predictors of Treatment Response in Primary Nephrotic Syndrome.Kidney medicine · 2026Article
- The importance of the degree of foot process effacement in evaluating the prognosis of IgA nephropathy.International urology and nephrology · 2025Article
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- Hidden genetics behind glomerular scars: an opportunity to understand the heterogeneity of focal segmental glomerulosclerosis?Pediatric nephrology (Berlin, Germany) · 2024Review
- Characterizing Glomerular Barrier Dysfunction with Patient-Derived Serum in Glomerulus-on-a-Chip Models: Unveiling New Insights into Glomerulonephritis.International journal of molecular sciences · 2024Article
- A new index for the outcome of focal segmental glomerulosclerosis.Scientific reports · 2024Article
- Dach1 is essential for maintaining normal mature podocytes.PloS one · 2024Article
- The Therapeutic Mechanisms of Shenyan Oral Liquid I Against Chronic Kidney Disease Based on Network Pharmacology and Experimental Validation.Combinatorial chemistry & high throughput screening · 2024Article
- Early growth response 1 as a podocyte injury marker in human glomerular diseases.Clinical kidney journal · 2024Article
- Placental Mesenchymal Stem Cells Alleviate Podocyte Injury in Diabetic Kidney Disease by Modulating Mitophagy via the SIRT1-PGC-1alpha-TFAM Pathway.International journal of molecular sciences · 2023Article
- Article
- Podocytes are lost from glomeruli before completing apoptosis.American journal of physiology. Renal physiology · 2022Article
- Protective effects of rituximab on puromycin-induced apoptosis, loss of adhesion and cytoskeletal alterations in human podocytes.Scientific reports · 2022Article
- A novel unbiased method reveals progressive podocyte globotriaosylceramide accumulation and loss with age in females with Fabry disease.Kidney international · 2022Article
- Kidney injury-mediated disruption of intestinal lymphatics involves dicarbonyl-modified lipoproteins.Kidney international · 2021Article
- CMIP interacts with WT1 and targets it on the proteasome degradation pathway.Clinical and translational medicine · 2021Article
- Indirect podocyte injury manifested in a partial podocytectomy mouse model.American journal of physiology. Renal physiology · 2021Article
- Nicotine, smoking, podocytes, and diabetic nephropathy.American journal of physiology. Renal physiology · 2021Article
- Controversies in Podocyte Loss: Death or Detachment?Frontiers in cell and developmental biology · 2021Review
6 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
Loss of podocytes promotes glomerulosclerosis, but whether this results from a continued primary insult or a secondary mechanism triggered by the initial loss of podocytes is unknown. We generated chimeric mice in which only a subpopulation of podocytes expressed hCD25, which is the receptor for the immunotoxin LMB2. In addition, genetic labeling of hCD25-negative cells with human placental alkaline phosphatase allowed the study of these two distinct podocyte populations. Administration of LMB2 did not cause podocyte injury in hCD25-negative control mice. In contrast, LMB2 severely damaged or sloughed off the subpopulation of hCD25-positive podocytes within the chimeric glomeruli. Moreover, hCD25-negative podocytes, which were immune to the initial toxin injury, developed injury as early as 4 d after LMB2 injection, evidenced by foot process effacement, upregulation of desmin, and downregulation of nephrin, podocin, and podocalyxin. Furthermore, the magnitude of secondary injury correlated with the magnitude of primary injury, supporting the concept of an amplified cascade of podocyte injury. In conclusion, podocyte damage can propagate injury by triggering secondary damage of "remnant" intact podocytes, even when the primary insult is short-lived. This transmission of podocyte injury may form a vicious cycle leading to accelerated podocyte deterioration and glomerulosclerosis.
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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 Socratic graph.