ReviewJournal of pathology and translational medicine2016
Pathogenesis of Focal Segmental Glomerulosclerosis.
Review in Journal of pathology and translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 58 citations in OpenAlex.
- Predictive Molecular Biomarkers in Pediatric Steroid-Resistant Nephrotic Syndrome: A Systematic Review.International journal of nephrology and renovascular disease · 2026Review
- Focal Segmental Glomerulosclerosis: Comprehensive Review and Exploration of the Dual Potential of Cyclodextrins in Therapeutic Optimization.International journal of molecular sciences · 2025Review
- Article
- Clinical implications of apolipoprotein L1 testing in patients with focal segmental glomerulosclerosis: a review of diagnostic and prognostic implications.Annals of medicine and surgery (2012) · 2025Review
- Purinergic Receptor Activation Protects Glomerular Microvasculature from Increased Mechanical Stress in Angiotensin II-Induced Hypertension: A Modeling Study.International journal of molecular sciences · 2025Article
- Article
- Rituximab in the treatment of primary FSGS: time for its use in routine clinical practice?Clinical kidney journal · 2023Article
- High Rate of Mutations of Adhesion Molecules and Extracellular Matrix Glycoproteins in Patients with Adult-Onset Focal and Segmental Glomerulosclerosis.Biomedicines · 2023Article
- Calcineurin inhibitors or cyclophosphamide in the treatment of membranous nephropathy superimposed with FSGS lesions: a retrospective study from China.Renal failure · 2023Article
- The role of HLA antigens in recurrent primary focal segmental glomerulosclerosis.Frontiers in immunology · 2023Article
- Article
- Monogenic focal segmental glomerulosclerosis: A conceptual framework for identification and management of a heterogeneous disease.American journal of medical genetics. Part C, Seminars in medical genetics · 2022Review
- CD44-negative parietal-epithelial cell staining in minimal change disease: association with clinical features, response to corticosteroids and kidney outcome.Clinical kidney journal · 2022Article
- The recruitment mechanisms and potential therapeutic targets of podocytes from parietal epithelial cells.Journal of translational medicine · 2021Review
- Recessive, gain-of-function toxicity in an APOL1 BAC transgenic mouse model mirrors human APOL1 kidney disease.Disease models & mechanisms · 2021Article
- MRTF: Basic Biology and Role in Kidney Disease.International journal of molecular sciences · 2021Review
- A novel heterozygous variant of the COL4A4 gene in a Chinese family with hematuria and proteinuria leads to focal segmental glomerulosclerosis and chronic kidney disease.Molecular genetics & genomic medicine · 2020Article
- Review
- Non-ischemic cardiomyopathy with focal segmental glomerulosclerosis.Journal of community hospital internal medicine perspectives · 2020Article
- Renal progenitor cells modulated by angiotensin II receptor blocker (ARB) medication and differentiation towards podocytes in anti-thy1.1 nephritis.Annals of translational medicine · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Focal segmental glomerulosclerosis (FSGS) is characterized by focal and segmental obliteration of glomerular capillary tufts with increased matrix. FSGS is classified as collapsing, tip, cellular, perihilar and not otherwise specified variants according to the location and character of the sclerotic lesion. Primary or idiopathic FSGS is considered to be related to podocyte injury, and the pathogenesis of podocyte injury has been actively investigated. Several circulating factors affecting podocyte permeability barrier have been proposed, but not proven to cause FSGS. FSGS may also be caused by genetic alterations. These genes are mainly those regulating slit diaphragm structure, actin cytoskeleton of podocytes, and foot process structure. The mode of inheritance and age of onset are different according to the gene involved. Recently, the role of parietal epithelial cells (PECs) has been highlighted. Podocytes and PECs have common mesenchymal progenitors, therefore, PECs could be a source of podocyte repopulation after podocyte injury. Activated PECs migrate along adhesion to the glomerular tuft and may also contribute to the progression of sclerosis. Markers of activated PECs, including CD44, could be used to distinguish FSGS from minimal change disease. The pathogenesis of FSGS is very complex; however, understanding basic mechanisms of podocyte injury is important not only for basic research, but also for daily diagnostic pathology practice.
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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.