ArticlePloS one2015
The Accumulation of VEGFA in the Glomerular Basement Membrane and Its Relationship with Podocyte Injury and Proteinuria in Alport Syndrome.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Potential Renal Damage Biomarkers in Alport Syndrome-A Review of the Literature.International journal of molecular sciences · 2022Pooled it
- Extracellular vesicle miR-93-5p cargo regulates glomerular endothelial cell damage in Alport syndrome.JCI insight · 2026Article
- Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Mechanisms and Therapeutic Perspectives of Podocyte Aging in Podocytopathies.International journal of molecular sciences · 2025Review
- MicroRNAs in idiopathic childhood nephrotic syndrome.Clinical and experimental nephrology · 2025Article
- Case Report: Nephrotic syndrome as the primary manifestation of Alport syndrome in a Chinese pediatric patient.Frontiers in pediatrics · 2024Article
- Glomerular cell cross talk in diabetic kidney diseases.Journal of diabetes · 2022Review
- Synaptopodin deficiency exacerbates kidney disease in a mouse model of Alport syndrome.American journal of physiology. Renal physiology · 2021Article
- Nephrotoxicity of Anti-Angiogenic Therapies.Diagnostics (Basel, Switzerland) · 2021Review
- Network pharmacology modeling identifies synergistic interaction of therapeutic and toxicological mechanisms for Tripterygium hypoglaucum Hutch.BMC complementary medicine and therapies · 2021Article
- Molecular and functional characterization of urine-derived podocytes from patients with Alport syndrome.The Journal of pathology · 2020Article
- Article
- Establishment of microRNA, transcript and protein regulatory networks in Alport syndrome induced pluripotent stem cells.Molecular medicine reports · 2019Article
- Amniotic fluid stem cell-derived vesicles protect from VEGF-induced endothelial damage.Scientific reports · 2017Article
- Targeted delivery of celastrol to mesangial cells is effective against mesangioproliferative glomerulonephritis.Nature communications · 2017Article
- Hyperactive FOXO1 results in lack of tip stalk identity and deficient microvascular regeneration during kidney injury.Biomaterials · 2017Article
- Glomerular cell crosstalk.Current opinion in nephrology and hypertension · 2016Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of proteinuria in Alport syndrome (AS) remains unclear. Vascular endothelial growth factor A (VEGFA) is a key regulator of the glomerular filtration barrier (GFB). This study explored the expression of VEGFA in the glomeruli and its accumulation in the glomerular basement membrane (GBM) and their relationship with podocyte injury and proteinuria in Alport syndrome (AS). Clinical data and renal tissues of control patients (11 cases) and AS patients (25 cases) were included. AS patients were further divided into 2 groups according to the quantities of their urinary protein: mild to moderate proteinuria group (proteinuria <50 mg/kg/d, 15 cases) and heavy proteinuria group (proteinuria ≥50 mg/kg/d, 10 cases). The expression and distribution of VEGFA and VEGF receptor 2 (VEGFR2) in the GFB, the phosphorylation of VEGFR2 (p-VEGFR2) and nephrin (p-nephrin), and the expression of synaptopodin and nephrin in the glomeruli were detected by immune electron microscopy and/or immunofluorescence, and their relationships to proteinuria in AS patients were analyzed. The accumulation of VEGFA in the GBM was increased in AS patients. The expression of VEGFA and the levels of p-VEGFR2 and p-nephrin in glomeruli were increased and were positively correlated with the degree of proteinuria in AS patients. The expression of synaptopodin and nephrin were decreased and were negatively correlated with the degree of proteinuria in AS patients. The over expressed VEGFA in the glomeruli and its accumulation in the GBM may activate the VEGFA-VEGFR2 and nephrin signaling pathways and lead to podocyte injury and occurrence of proteinuria in AS.
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