ArticleBioMed research international2015
Early-onset diabetic E1-DN mice develop albuminuria and glomerular injury typical of diabetic nephropathy.
Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Renal Biomarkers as Predictors of Renal Damage in Patients With Type 2 Diabetes.BioMed research international · 2026Article
- Adiponectin receptor agonist AdipoRon ameliorates renal inflammation in diet-induced obese mice and endotoxin-treated human glomeruli ex vivo.Diabetologia · 2021Article
- Metformin Protects against Podocyte Injury in Diabetic Kidney Disease.Pharmaceuticals (Basel, Switzerland) · 2020Review
- SHIPping out diabetes-Metformin, an old friend among new SHIP2 inhibitors.Acta physiologica (Oxford, England) · 2020Review
- Mesenchymal Stem Cell Therapy for Diabetic Kidney Disease: A Review of the Studies Using Syngeneic, Autologous, Allogeneic, and Xenogeneic Cells.Stem cells international · 2020Review
- Article
- Glucose Transporters in Diabetic Kidney Disease-Friends or Foes?Frontiers in endocrinology · 2018Review
- PACSIN2 accelerates nephrin trafficking and is up-regulated in diabetic kidney disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Mesenchymal Stem Cells as Therapeutic Candidates for Halting the Progression of Diabetic Nephropathy.Stem cells international · 2016Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
The transgenic E1-DN mice express a kinase-negative epidermal growth factor receptor in their pancreatic islets and are diabetic from two weeks of age due to impaired postnatal growth of β-cell mass. Here, we characterize the development of hyperglycaemia-induced renal injury in the E1-DN mice. Homozygous mice showed increased albumin excretion rate (AER) at the age of 10 weeks; the albuminuria increased over time and correlated with blood glucose. Morphometric analysis of PAS-stained histological sections and electron microscopy images revealed mesangial expansion in homozygous E1-DN mice, and glomerular sclerosis was observed in the most hyperglycaemic mice. The albuminuric homozygous mice developed also other structural changes in the glomeruli, including thickening of the glomerular basement membrane and widening of podocyte foot processes that are typical for diabetic nephropathy. Increased apoptosis of podocytes was identified as one mechanism contributing to glomerular injury. In addition, nephrin expression was reduced in the podocytes of albuminuric homozygous E1-DN mice. Tubular changes included altered epithelial cell morphology and increased proliferation. In conclusion, hyperglycaemic E1-DN mice develop albuminuria and glomerular and tubular injury typical of human diabetic nephropathy and can serve as a new model to study the mechanisms leading to the development of diabetic nephropathy.
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