ReviewFrontiers in endocrinology2014
Genes and podocytes - new insights into mechanisms of podocytopathy.
Review in Frontiers in endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- The Italian Society for Pediatric Nephrology (SINePe) consensus document on the management of nephrotic syndrome in children: Part I - Diagnosis and treatment of the first episode and the first relapse.Italian journal of pediatrics · 2017Pooled it
- PLCε regulates podocyte differentiation and TGF-β1 responses via alteration of SMAD2/SMAD3 ratio.Cell communication and signaling : CCS · 2026Article
- CDKAL1 dysfunction impairs lysine codon translation in podocytes and accelerates chronic kidney disease.The EMBO journal · 2026Article
- Epigenetic mechanisms and steroid-resistant nephrotic syndrome: The future potential for SRNS diagnosis.iScience · 2026Review
- Reconstruction of Single-Cell Spatial Transcriptomes in Archival Kidney Biopsies.Kidney international reports · 2026Article
- Review
- Genetic etiology of inherited kidney diseases in egyptian patients: next generation sequencing identifies six novel variants.Molecular and cellular pediatrics · 2025Article
- Revisiting nephrin signaling and its specialized effects on the uniquely adaptable podocyte.The Biochemical journal · 2025Review
- Transcriptional Regulators YAP and TAZ Have Distinct Abilities to Compensate for One Another in Podocytes.Journal of the American Society of Nephrology : JASN · 2025Article
- Minimal Change Disease with Progression to Focal Segmental Glomerulosclerosis: Support for an Immune-Mediated Disease Continuum.Journal of Brown hospital medicine · 2025Article
- Integrative analysis of multi-omics data reveals importance of collagen and the PI3K AKT signalling pathway in CAKUT.Scientific reports · 2024Article
- Steroid-Resistant Nephrotic Syndrome due toKidney international reports · 2024Article
- Modeling Podocyte Ontogeny and Podocytopathies with the Zebrafish.Journal of developmental biology · 2023Review
- Review
- Tripartite Separation of Glomerular Cell Types and Proteomes from Reporter-Free Mice.Journal of the American Society of Nephrology : JASN · 2021Article
- Transcription factor Kruppel-like factor 5 positively regulates the expression of AarF domain containing kinase 4.Molecular biology reports · 2020Article
- A case report of adult-onset COQ8B nephropathy presenting focal segmental glomerulosclerosis with granular swollen podocytes.BMC nephrology · 2020Article
- Centromere protein I (CENPI) is a candidate gene for X-linked steroid sensitive nephrotic syndrome.Journal of nephrology · 2020Article
- Podocytopathy and Nephrotic Syndrome in Mice with Podocyte-Specific Deletion of the Asah1 Gene: Role of Ceramide Accumulation in Glomeruli.The American journal of pathology · 2020Article
- Expression Levels of miR-30c and miR-186 in Adult Patients with Membranous Glomerulonephritis and Focal Segmental Glomerulosclerosis.International journal of nephrology and renovascular disease · 2020Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
After decades of primarily morphological study, positional cloning of the NPHS1 gene was the landmark event that established aberrant podocyte genetics as a pivotal cause of malfunction of the glomerular filter. This ended any uncertainty whether genetic mutation plays a significant role in hereditary nephrotic syndromes (NS) and confirmed podocytes as critical players in regulating glomerular protein filtration. Although subsequent sequencing of candidate genes chosen on the basis of podocyte biology had less success, unbiased analysis of genetically informative kindreds and syndromic disease has led to further gene discovery. However, the 45 genes currently associated with human NS explain not more than 20-30% of hereditary and only 10-20% of sporadic cases. It is becoming increasingly clear both from genetic analysis and phenotypic data - including occasional response to immunosuppressive agents and post-transplant disease recurrence in Mendelian disease - that monogenic inheritance of abnormalities in podocyte-specific genes disrupting filter function is only part of the story. Recent advances in genetic screening technology combined with increasingly robust bioinformatics are set to allow identification and characterization of novel disease causing variants and more importantly, disease modifying genes. Emerging data also support a significant but incompletely characterized immunoregulatory component.
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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.