ArticleBiochimie2020
EDA2R mediates podocyte injury in high glucose milieu.
Article in Biochimie, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- X-chromosome and kidney function: evidence from a multi-trait genetic analysis of 908,697 individuals reveals sex-specific and sex-differential findings in genes regulated by androgen response elements.Nature communications · 2024Pooled it
- Proteomic signature of dementia risk in type 2 diabetes.Journal of advanced research · 2026Article
- Preterm Birth Increases Susceptibility to Hyperglycemia-Induced Kidney Injury With Sex-Specific Differences in Structural and Molecular Responses.Endocrinology, diabetes & metabolism · 2026Article
- ORANGE: a machine learning approach for modeling tissue-specific aging from transcriptomic data.Briefings in bioinformatics · 2026Article
- The Roles of EDA2R in Ageing and Disease.Aging cell · 2025Review
- Multiple circulating inflammatory proteins are associated with pathological lesions and kidney function decline in IgA nephropathy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Spatial and Temporal Expression Patterns of EDA2R, PCDH9, and TRAF7 inInternational journal of molecular sciences · 2025Article
- Elevated reactive oxygen species can drive the alternative lengthening of telomeres pathway in ATRX-null cancers.Nucleic acids research · 2025Article
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
- RNA-Seq transcriptome profiling of Nile rat livers reveals novel insights on the anti-diabetic mechanisms of Water-Soluble Palm Fruit Extract.Journal of applied genetics · 2024Article
- Ectodysplasin-A2 receptor (EDA2R) knockdown alleviates myocardial ischemia/reperfusion injury through inhibiting the activation of the NF-κB signaling pathway.Experimental animals · 2024Article
- Expression of Congenital Anomalies of the Kidney and Urinary Tract (CAKUT) Candidate GenesGenes · 2024Article
- Decay of Skin-Specific Gene Modules in Pangolins.Journal of molecular evolution · 2023Article
- Nicotine exacerbates diabetic nephropathy through upregulation of Grem1 expression.Molecular medicine (Cambridge, Mass.) · 2023Article
- Association between Circulating Ectodysplasin A and Diabetic Kidney Disease.Journal of diabetes research · 2023Article
- Single-Nucleus Transcriptional Profiling of Chronic Kidney Disease after Cisplatin Nephrotoxicity.The American journal of pathology · 2022Article
- Molecular Mechanisms of Kidney Injury and Repair.International journal of molecular sciences · 2022Review
- Epigenetics and endoplasmic reticulum in podocytopathy during diabetic nephropathy progression.Frontiers in immunology · 2022Review
- Regulation of Podocyte Injury by CircHIPK3/FUS Complex in Diabetic Kidney Disease.International journal of biological sciences · 2022Article
- Ectodysplasin A/Ectodysplasin A Receptor System and Their Roles in Multiple Diseases.Frontiers in physiology · 2021Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
Abstract
EDA2R is a member of the large family of tumor necrosis factor receptor (TNFR). Previous studies suggested that EDA2R expression might be increased in the kidneys of diabetic mice. However, its mRNA and protein expression in kidneys were not analyzed; moreover, its role in the development of diabetic kidney disease was not explored. Here we analyzed the mRNA and protein expressions of EDA2R in diabetic kidneys and examined its role in the podocyte injury in high glucose milieu. By analysis with real-time PCR, Western blotting, we found that both the mRNA and protein levels of EDA2R were increased in the kidneys of diabetic mice. Immunohistochemical studies revealed that EDA2R expression was enhanced in both glomerular and tubular cells of diabetic mice and humans. In vitro studies, high glucose increased EDA2R expression in cultured human podocytes. Overexpression of EDA2R in podocytes promoted podocyte apoptosis and decreased nephrin expression. Moreover, ED2AR increased ROS generation in podocytes, while inhibiting ROS generation attenuates EDA2R-mediated podocyte injury. In addition, EDA2R silencing partially suppressed high glucose-induced ROS generation, apoptosis, and nephrin decrease. Our study demonstrated that high glucose increases EDA2R expression in kidney cells and that EDA2R induces podocyte apoptosis and dedifferentiation in high glucose milieu partially through enhanced ROS generation.
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