ReviewBMC nephrology2013
Pathophysiology and treatment of focal segmental glomerulosclerosis: the role of animal models.
Review in BMC nephrology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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
22 citing papers in PubMed, 52 citations in OpenAlex.
- Dapagliflozin in focal segmental glomerulosclerosis: a combined human-rodent pilot study.American journal of physiology. Renal physiology · 2018Trial
- Inflammation in glomerular diseases.Frontiers in immunology · 2025Review
- Polycystic Ovary Syndrome Accompanied by Hyperandrogenemia or Metabolic Syndrome Triggers Glomerular Podocyte Injury.Diagnostics (Basel, Switzerland) · 2024Article
- Article
- Effect of Everolimus versus Bone Marrow-Derived Stem Cells on Glomerular Injury in a Rat Model of Glomerulonephritis: A Preventive, Predictive and Personalized Implication.International journal of molecular sciences · 2021Article
- A comprehensive analysis of NPHS1 gene mutations in patients with sporadic focal segmental glomerulosclerosis.BMC medical genetics · 2019Article
- Chondroitin sulfate degradation and eicosanoid metabolism pathways are impaired in focal segmental glomerulosclerosis: Experimental confirmation of anBioImpacts : BI · 2019Article
- Recent advances of animal model of focal segmental glomerulosclerosis.Clinical and experimental nephrology · 2018Review
- Kidney disease models: tools to identify mechanisms and potential therapeutic targets.Zoological research · 2018Review
- Article
- Klotho suppresses the renin-angiotensin system in adriamycin nephropathy.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2017Article
- Multiple Targets for Novel Therapy of FSGS Associated with Circulating Permeability Factor.BioMed research international · 2017Review
- Interferon Induced Focal Segmental Glomerulosclerosis.Case reports in nephrology · 2016Article
- Soluble Urokinase Receptors in Focal Segmental Glomerulosclerosis: A Review on the Scientific Point of View.Journal of immunology research · 2016Review
- Cells of renin lineage are adult pluripotent progenitors in experimental glomerular disease.American journal of physiology. Renal physiology · 2015Article
- The influences of larger physical constitutions including obesity on the amount of urine protein excretion in primary glomerulonephritis: research of the Japan Renal Biopsy Registry.Clinical and experimental nephrology · 2015Article
- Novel therapies for FSGS: preclinical and clinical studies.Advances in chronic kidney disease · 2015Review
- Article
- Transgenic Strategies to Study Podocyte Loss and Regeneration.Stem cells international · 2015Review
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Focal segmental glomerulosclerosis (FSGS) is a kidney disease with progressive glomerular scarring and a clinical presentation of nephrotic syndrome. FSGS is a common primary glomerular disorder that causes renal dysfunction which progresses slowly over time to end-stage renal disease. Most cases of FSGS are idiopathic Although kidney transplantation is a potentially curative treatment, 40% of patients have recurrence of FSGS after transplantation. In this review a brief summary of the pathogenesis causing FSGS in humans is given, and a variety of animal models used to study FSGS is discussed. These animal models include the reduction of renal mass by resecting 5/6 of the kidney, reduction of renal mass due to systemic diseases such as hypertension, hyperlipidemia or SLE, drug-induced FSGS using adriamycin, puromycin or streptozotocin, virus-induced FSGS, genetically-induced FSGS such as via Mpv-17 inactivation and α-actinin 4 and podocin knockouts, and a model for circulating permeability factors. In addition, an animal model that spontaneously develops FSGS is discussed. To date, there is no exact understanding of the pathogenesis of idiopathic FSGS, and there is no definite curative treatment. One requirement facilitating FSGS research is an animal model that resembles human FSGS. Most animal models induce secondary forms of FSGS in an acute manner. The ideal animal model for primary FSGS, however, should mimic the human primary form in that it develops spontaneously and has a slow chronic progression. Such models are currently not available. We conclude that there is a need for a better animal model to investigate the pathogenesis and potential treatment options of FSGS.
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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.