ArticleMolecular and cellular biology2004
Early glomerular filtration defect and severe renal disease in podocin-deficient mice.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
98 citing papers in PubMed, 261 citations in OpenAlex.
- CDKAL1 dysfunction impairs lysine codon translation in podocytes and accelerates chronic kidney disease.The EMBO journal · 2026Article
- Clinical Presentation, Genetic Testing, and Outcome of Congenital Nephrotic Syndrome in KwaZulu-Natal, South Africa.Nephron · 2026Article
- Mechanosensitive Differentiation of Human iPS Cell-Derived Podocytes.Bioengineering (Basel, Switzerland) · 2024Article
- Glucosylceramide synthase modulation ameliorates murine renal pathologies and promotes macrophage effector function in vitro.Communications biology · 2024Article
- Correlative multiphoton-STED microscopy of podocyte calcium levels and slit diaphragm ultrastructure in the renal glomerulus.Scientific reports · 2024Article
- Quantitative phenotyping ofAmerican journal of physiology. Renal physiology · 2024Article
- Steroid-Resistant Nephrotic Syndrome due toKidney international reports · 2024Article
- In vivo characterization of a podocyte-expressed short podocin isoform.BMC nephrology · 2023Article
- Article
- Mapping of the podocin proximity-dependent proteome reveals novel components of the kidney podocyte foot process.Frontiers in cell and developmental biology · 2023Article
- A slit-diaphragm-associated protein network for dynamic control of renal filtration.Nature communications · 2022Article
- Article
- A critical re-analysis of cases of post-transplantation recurrence in genetic nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2021Article
- Podocyte-specific Crb2 knockout mice develop focal segmental glomerulosclerosis.Scientific reports · 2021Article
- Interleukin 37 (IL-37) Reduces High Glucose-Induced Inflammation, Oxidative Stress, and Apoptosis of Podocytes by Inhibiting the STAT3-Cyclophilin A (CypA) Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Repeated Administration of Clinical Doses of Tramadol and Tapentadol Causes Hepato- and Nephrotoxic Effects in Wistar Rats.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Disease Modeling To Understand the Pathomechanisms of Human Genetic Kidney Disorders.Clinical journal of the American Society of Nephrology : CJASN · 2020Review
- Altered renal hemodynamics is associated with glomerular lipid accumulation in obese Dahl salt-sensitive leptin receptor mutant rats.American journal of physiology. Renal physiology · 2020Article
- Injured Podocytes Are Sensitized to Angiotensin II-Induced Calcium Signaling.Journal of the American Society of Nephrology : JASN · 2020Article
- Critical roles of PI3K/Akt/NF‑κB survival axis in angiotensin II‑induced podocyte injury.Molecular medicine reports · 2019Article
38 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Podocytes are specialized epithelial cells covering the basement membrane of the glomerulus in the kidney. The molecular mechanisms underlying the role of podocytes in glomerular filtration are still largely unknown. We generated podocin-deficient (Nphs2-/-) mice to investigate the function of podocin, a protein expressed at the insertion of the slit diaphragm in podocytes and defective in a subset of patients with steroid-resistant nephrotic syndrome and focal and segmental glomerulosclerosis. Nphs2-/- mice developed proteinuria during the antenatal period and died a few days after birth from renal failure caused by massive mesangial sclerosis. Electron microscopy revealed the extensive fusion of podocyte foot processes and the lack of a slit diaphragm in the remaining foot process junctions. Using real-time PCR and immunolabeling, we showed that the expression of other slit diaphragm components was modified in Nphs2-/- kidneys: the expression of the nephrin gene was downregulated, whereas that of the ZO1 and CD2AP genes appeared to be upregulated. Interestingly, the progression of the renal disease, as well as the presence or absence of renal vascular lesions, depends on the genetic background. Our data demonstrate the crucial role of podocin in the establishment of the glomerular filtration barrier and provide a suitable model for mapping and identifying modifier genes involved in glomerular diseases caused by podocyte injuries.
Indexed as
Identifiers
What OpenQuestion holds
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.