ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2021
Epidermal Growth Factor Protects Against High Glucose-Induced Podocyte Injury Possibly via Modulation of Autophagy and PI3K/AKT/mTOR Signaling Pathway Through DNA Methylation.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- Dynamic Changes of Selected Signaling Molecules in Ovaries Following Early-Life Exposure to Fumonisin B1 in Wistar Rats in Association With DNA Methylation.Physiological research · 2025Article
- Cellular and Molecular Resolution of Focal Segmental Glomerulosclerosis Recurrence in Human Allografts.bioRxiv : the preprint server for biology · 2025Article
- Immune-mediated renal injury in diabetic kidney disease: from mechanisms to therapy.Frontiers in immunology · 2025Review
- Advances in the Epigenetic Mechanisms of Diabetic Nephropathy Pathogenesis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Review
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
- Mechanisms and cross-talk of regulated cell death and their epigenetic modifications in tumor progression.Molecular cancer · 2024Review
- Identification of key immune-related genes and potential therapeutic drugs in diabetic nephropathy based on machine learning algorithms.BMC medical genomics · 2024Article
- Article
- Investigating EGF and PAG1 as necroptosis-related biomarkers for diabetic nephropathy: anAging · 2023Article
- Acteoside protects podocyte against apoptosis through regulating AKT/GSK-3β signaling pathway in db/db mice.BMC endocrine disorders · 2023Article
- Urinary epidermal growth factor predicts complete remission of proteinuria in Chinese children with IgA nephropathy.Pediatric research · 2023Article
- Clinical application of RUBCN/SESN2 mediated inhibition of autophagy as biomarkers of diabetic kidney disease.Molecular medicine (Cambridge, Mass.) · 2022Article
- Observational
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7 authors at 4 institutions in 1 country.
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Abstract
aimDiabetic nephropathy (DN) is a serious health problem worldwide. Epidermal growth factor (EGF) has suggested as a potential biomarker for the progression of chronic kidney disease. In this study, we examined the effects of EGF on the high glucose (HG)-induced podocyte injury and explored the underlying molecular mechanisms.
methodsThe cell proliferation, toxicity, and cell apoptosis of podocytes were determined by CCK-8 assay, lactate dehydrogenase release assay, and flow cytometry, respectively, and protein levels in the podocytes were determined by Western blot assay. Mechanistically, DNA methylation analysis, bioinformatic analysis, methylation‑specific PCR and quantitative real-time PCR were used to analyze functional pathways in differentially methylated genes and the expression of the key methylated genes in the podocytes after different interventions.
resultsEGF treatment significantly increased the protein expression level of LC3 and decreased the protein level of P62 in HG-stimulated podocytes, which was attenuated by autophagy inhibitor, 3-methyladenine. EGF increased the cell proliferation and the protein expression levels of nephrin and synaptopodin, but reduced cell toxicity and cell apoptosis and protein expression level of cleaved caspase-3, which was partially antagonized by 3-methyladenine. DNA methylation expression profiles revealed the differential hypermethylation sites and hypomethylation sites among podocytes treated with normal glucose, HG and HG+EGF. GO enrichment analysis showed that DNA methylation was significantly enriched in negative regulation of phosphorylation, cell-cell junction and GTPase binding. KEGG pathway analysis showed that these genes were mainly enriched in PI3K-Akt, Hippo and autophagy pathways. Further validation studies revealed that six hub genes (ITGB1, GRB2, FN1, ITGB3, FZD10 and FGFR1) may be associated with the protective effects of EGF on the HG-induced podocyte injury.
conclusionIn summary, our results demonstrated that EGF exerted protective effects on HG-induced podocytes injury via enhancing cell proliferation and inhibiting cell apoptosis. Further mechanistic studies implied that EGF-mediated protective effects in HG-stimulated podocytes may be associated with modulation of autophagy and PI3K/AKT/mTOR signaling pathway.
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