ArticleJournal of molecular histology2020
Down-regulation of SETD6 protects podocyte against high glucose and palmitic acid-induced apoptosis, and mitochondrial dysfunction via activating Nrf2-Keap1 signaling pathway in diabetic nephropathy.
Article in Journal of molecular histology, 2020. 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, 21 citations in OpenAlex.
- Intervention Value of Path-Type Health Education on Cognition and Renal Function of Patients with Diabetic Nephropathy.Computational and mathematical methods in medicine · 2021Trial
- MYO1C is a urinary extracellular vesicle biomarker and mediator of podocyte injury in diabetic nephropathy.JCI insight · 2026Article
- Orchestrating epigenetics: a comprehensive review of the methyltransferase SETD6.Experimental & molecular medicine · 2025Review
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
- Roles of Mitochondrial Dysfunction in Diabetic Kidney Disease: New Perspectives from Mechanism to Therapy.Biomolecules · 2024Review
- Icariin synergizes therapeutic effect of dexamethasone on adriamycin-induced nephrotic syndrome.European journal of medical research · 2023Article
- TDAG51-Deficiency Podocytes are Protected from High-Glucose-Induced Damage Through Nrf2 Activation via the AKT-GSK-3β Pathway.Inflammation · 2022Article
- Methyltransferase SET domain family and its relationship with cardiovascular development and diseases.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022Article
- Therapeutic potential of Nrf-2 pathway in the treatment of diabetic neuropathy and nephropathy.Molecular biology reports · 2021Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Diabetic nephropathy (DN), a serious complication of hyperglycemia, is one of the most common causes of end-stage renal disease (ESRD). Glomerular podocyte injury is a major mechanism that leads to DN. However, the mechanisms underlying podocyte injury are ambiguous. In this study, we sought to investigate the contribution of SET domain-containing protein 6 (SETD6) to the pathogenesis of podocyte injury induced by glucose (GLU) and palmitic acid (PA), as well as the underlying mechanisms. Our results showed that GLU and PA treatment significantly decreased SETD6 expression in mouse podocytes. Besides, Cell Counting Kit-8 (CCK-8) and flow cytometry assay demonstrated that silencing of SETD6 silence obviously enhanced cell viability, and suppressed apoptosis in GLU and PA-induced podocytes. We also discovered that downregulation of SETD6 suppressed GLU and PA-induced ROS generation and podocyte mitochondrial dysfunction. Nrf2-Keap1 signaling pathway was involved in the effect of SETD6 on mitochondrial dysfunction. Taken together, silencing of SETD6 protected mouse podocyte against apoptosis and mitochondrial dysfunction through activating Nrf2-Keap1 signaling pathway. Therefore these data provide new insights into new potential therapeutic targets for DN treatment.
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