ArticleThe American journal of pathology2017
High Glucose-Induced Hypomethylation Promotes Binding of Sp-1 to Myo-Inositol Oxygenase: Implication in the Pathobiology of Diabetic Tubulopathy.
Article in The American journal of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 36 citations in OpenAlex.
- Metformin alleviates renal tubular injury in diabetic kidney disease by activating mitophagy and inhibiting ferroptosis via HIF-1α/MIOX axis.Journal of pharmaceutical analysis · 2025Article
- Myo-Inositol Oxygenase (MIOX): A Pivotal Regulator and Therapeutic Target in Multiple Diseases.Current issues in molecular biology · 2025Review
- PTEN: A Novel Diabetes Nephropathy Protective Gene Related to Cellular Senescence.International journal of molecular sciences · 2025Article
- Identification of biomarkers and mechanism exploration of ferroptosis related genes regulated by m6A in type 2 diabetes mellitus.Hereditas · 2025Article
- Review
- Targeting the Epigenetic Marks in Type 2 Diabetes Mellitus: Will Epigenetic Therapy Be a Valuable Adjunct to Pharmacotherapy?Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Article
- Nox4 as a novel therapeutic target for diabetic vascular complications.Redox biology · 2023Review
- Epigenetics of the Pathogenesis and Complications of Type 2 Diabetes Mellitus.TouchREVIEWS in endocrinology · 2023Review
- Symbiotic microbes aid host adaptation by metabolizing a deterrent host pine carbohydrate d-pinitol in a beetle-fungus invasive complex.Science advances · 2022Article
- Article
- Epigenetics in the pathogenesis of diabetic nephropathy.Acta biochimica et biophysica Sinica · 2022Review
- Cellular Senescence and Regulated Cell Death of Tubular Epithelial Cells in Diabetic Kidney Disease.Frontiers in endocrinology · 2022Review
- Transcription Factor ChREBP Mediates High Glucose-Evoked Increase in HIF-1α Content in Epithelial Cells of Renal Proximal Tubules.International journal of molecular sciences · 2021Article
- Bioinformatics analysis of genes related to iron death in diabetic nephropathy through network and pathway levels based approaches.PloS one · 2021Article
- Epigenetics in kidney diseases.Advances in clinical chemistry · 2021Review
- Acute Kidney Injury in Pediatric Diabetic Kidney Disease.Frontiers in pediatrics · 2021Review
- Kidney-based in vivo model for drug-induced nephrotoxicity testing.Scientific reports · 2020Article
- Circular RNA-ZNF532 regulates diabetes-induced retinal pericyte degeneration and vascular dysfunction.The Journal of clinical investigation · 2020Article
- Epigenetic Modifiers as Potential Therapeutic Targets in Diabetic Kidney Disease.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The catabolic enzyme myo-inositol oxygenase (MIOX) is expressed in proximal tubules and up-regulated in the diabetic state. Previously, we reported its transcriptional and translation regulation by high glucose (HG), osmolytes, and fatty acids. However, its epigenetic regulation is unknown. Bisulfite sequencing revealed that both human and mouse MIOX promoters, enriched with CpG sites, are hypomethylated and unmethylated under HG ambience and hyperglycemic states associated with increased MIOX expression. Eletrophoretic mobility shift assays revealed increased binding of unmethylated oligos with nucleoproteins of cells maintained under HG. In addition, a strong binding of specificity protein (Sp)-1 transcription factor with MIOX promoter was observed under HG, especially with unmethylated Sp-1 oligo. Specificity of binding was established by supershift assays and treatment with the Sp-1 inhibitor mithramycin. Promoter analysis revealed an increase in luciferase activity under HG, which was reduced after mutation of the Sp-1-binding site. Sp1 siRNA treatment reduced mRNA and protein expression of Sp-1 and MIOX and generation of reactive oxygen species derived from NADPH oxidase (NOX)-4 and mitochondrial sources. In addition, there was reduced expression of hypoxia-inducible factor-1α relevant in the pathogenesis of diabetic nephropathy. Sp1 siRNA treatment reduced fibronectin expression, an extracellular matrix protein that is increased in diabetic nephropathy and tubulopathy. HG-induced MIOX expression was also reduced with the treatment of apelin-13, which deacetylates histones. Overall, these findings highlight the epigenetic regulation of MIOX in the pathogenesis of diabetic tubulopathy.
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Registered trials
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