ArticleThe American journal of pathology2015
Glypican-5 Increases Susceptibility to Nephrotic Damage in Diabetic Kidney.
Article in The American journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Blood vessel remodeling in the cerebral cortex induced by binge alcohol intake in mice.Toxicological research · 2023Article
- Hedgehog pathway modulation by glypican 3-conjugated heparan sulfate.Journal of cell science · 2022Article
- Association of circulating fibroblast growth factor-2 with progression of HIV-chronic kidney diseases in children.Pediatric nephrology (Berlin, Germany) · 2021Article
- Integrated Environmental and Genomic Analysis Reveals the Drivers of Local Adaptation in African Indigenous Chickens.Molecular biology and evolution · 2021Article
- The Multiple Roles of Fibroblast Growth Factor in Diabetic Nephropathy.Journal of inflammation research · 2021Review
- Current updates on protein as biomarkers for diabetic kidney disease: a systematic review.Therapeutic advances in endocrinology and metabolism · 2021Review
- Genetic Disorders of the Glomerular Filtration Barrier.Clinical journal of the American Society of Nephrology : CJASN · 2020Review
- SHROOM3, the gene associated with chronic kidney disease, affects the podocyte structure.Scientific reports · 2020Article
- Proteoglycans in Obesity-Associated Metabolic Dysfunction and Meta-Inflammation.Frontiers in immunology · 2020Review
- APOL1 risk allele RNA contributes to renal toxicity by activating protein kinase R.Communications biology · 2018Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Type 2 diabetes mellitus is a leading health issue worldwide. Among cases of diabetes mellitus nephropathy (DN), the major complication of type 2 diabetes mellitus, the nephrotic phenotype is often intractable to clinical intervention and demonstrates the rapid decline of renal function to end-stage renal disease. We recently identified the gene for glypican-5 (GPC5), a cell-surface heparan sulfate proteoglycan, as conferring susceptibility for acquired nephrotic syndrome and additionally identified an association through a genome-wide association study between a variant in GPC5 and DN of type 2 diabetes mellitus. In vivo and in vitro data showed a progressive increase of GPC5 in type 2 DN along with severity; the excess was derived from glomerular mesangial cells. In this study, diabetic kidney showed that accumulation of fibroblast growth factor (Fgf)2 strikingly induced progressive proteinuria that was avoided in Gpc5 knockdown mice. The efficacy of Gpc5 inhibition was exerted through expression of the Fgf receptors 3 and 4 provoked in the diabetic kidney attributively. Extraglomerular Fgf2 was pathogenic in DN, and the deterrence of Gpc5 effectively inhibited the glomerular accumulation of Fgf2, the subsequent increase of mesangial extracellular matrix, and the podocytes' small GTPase activity. These findings elucidate the pivotal role of GPC5, identified as a susceptible gene in the genome-wide association study, in hyperglycemia-induced glomerulopathy.
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