ArticleJournal of the American Society of Nephrology : JASN2015
EGF receptor deletion in podocytes attenuates diabetic nephropathy.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.
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Who cites it
90 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.
- Disruption of podocyte cytoskeletal biomechanics by dasatinib leads to nephrotoxicity.Nature communications · 2019Pooled it
- The role of classical protein tyrosine phosphatases in diabetic kidney disease and therapeutic implications.Journal of biomedical science · 2026Review
- Article
- Malignant Transformation Risk in Patients With Oral Leukoplakia and Type 2 Diabetes Mellitus.International dental journal · 2026Article
- LncRNA GATA3-AS1-mediated miR-2116-5p interaction modulates TCF12 and contributes to podocyte dysfunction in childhood nephrotic syndrome.Clinics (Sao Paulo, Brazil) · 2026Article
- Analysis of high glucose injury using human induced pluripotent stem cell-derived kidney organoids.BMC nephrology · 2026Article
- TGF-β in chronic kidney disease: a controversy for decades.Frontiers in immunology · 2026Review
- Article
- Therapeutic role of Crateva religiosa in diabetic nephropathy: Insights into key signaling pathways.PloS one · 2025Article
- Multidimensional mechanisms of quercetin in diabetic kidney disease.Frontiers in cell and developmental biology · 2025Review
- Endothelial eNOS deficiency causes podocyte injury through NFAT2 and heparanase in diabetic mice.Scientific reports · 2024Article
- Vaccarin suppresses diabetic nephropathy through inhibiting the EGFR/ERK1/2 signaling pathway.Acta biochimica et biophysica Sinica · 2024Article
- Review
- Review
- "Qi Nan" agarwood restores podocyte autophagy in diabetic kidney disease by targeting EGFR signaling pathway.Chinese medicine · 2024Article
- Targeting the epidermal growth factor receptor (EGFR/ErbB) for the potential treatment of renal pathologies.Frontiers in pharmacology · 2024Review
- Metformin inhibits high glucose-induced apoptosis of renal podocyte through regulating miR-34a/SIRT1 axis.Immunity, inflammation and disease · 2024Article
- LncRNA HOX transcript antisense RNA mediates hyperglycemic-induced injury in the renal tubular epithelial cell via the miR-126-5pAkt axis.Aging medicine (Milton (N.S.W)) · 2023Article
- Article
- Glucose upregulates amphiregulin in oral dysplastic keratinocytes: A potential role in diabetes-associated oral carcinogenesis.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2023Article
30 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The generation of reactive oxygen species (ROS), particularly superoxide, by damaged or dysfunctional mitochondria has been postulated to be an initiating event in the development of diabetes complications. The glomerulus is a primary site of diabetic injury, and podocyte injury is a classic hallmark of diabetic glomerular lesions. In streptozotocin-induced type 1 diabetes, podocyte-specific EGF receptor (EGFR) knockout mice (EGFR(podKO)) and their wild-type (WT) littermates had similar levels of hyperglycemia and polyuria, but EGFR(podKO) mice had significantly less albuminuria and less podocyte loss compared with WT diabetic mice. Furthermore, EGFR(podKO) diabetic mice had less TGF-β1 expression, Smad2/3 phosphorylation, and glomerular fibronectin deposition. Immunoblotting of isolated glomerular lysates revealed that the upregulation of cleaved caspase 3 and downregulation of Bcl2 in WT diabetic mice were attenuated in EGFR(podKO) diabetic mice. Administration of the SOD mimetic mito-tempol or the NADPH oxidase inhibitor apocynin attenuated the upregulation of p-c-Src, p-EGFR, p-ERK1/2, p-Smad2/3, and TGF-β1 expression and prevented the alteration of cleaved caspase 3 and Bcl2 expression in glomeruli of WT diabetic mice. High-glucose treatment of cultured mouse podocytes induced similar alterations in the production of ROS; phosphorylation of c-Src, EGFR, and Smad2/3; and expression of TGF-β1, cleaved caspase 3, and Bcl2. These alterations were inhibited by treatment with mito-tempol or apocynin or by inhibiting EGFR expression or activity. Thus, results of our studies utilizing mice with podocyte-specific EGFR deletion demonstrate that EGFR activation has a major role in activating pathways that mediate podocyte injury and loss in diabetic nephropathy.
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