ArticleProceedings of the National Academy of Sciences of the United States of America2005
Modulation of renal-specific oxidoreductase/myo-inositol oxygenase by high-glucose ambience.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 58 citations in OpenAlex.
- Myo-inositol metabolism in two high-performance laying hen strains at different production periods.Poultry science · 2026Article
- 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
- Urine-derived renal tubular epithelial cells resemble functional characteristics of professional antigen-presenting cells and can directly induce BKV-specific T cell responses.Journal of nephrology · 2025Article
- Modulation of gentamicin-induced acute kidney injury by myo-inositol oxygenase via the ROS/ALOX-12/12-HETE/GPR31 signaling pathway.JCI insight · 2022Article
- Transcriptome Profiles Reveal a 12-Signature Metabolic Prediction Model and a Novel Role of Myo-Inositol Oxygenase in the Progression of Prostate Cancer.Frontiers in oncology · 2022Article
- Inositols Depletion and Resistance: Principal Mechanisms and Therapeutic Strategies.International journal of molecular sciences · 2021Review
- Excessively Enlarged Mitochondria in the Kidneys of Diabetic Nephropathy.Antioxidants (Basel, Switzerland) · 2021Review
- Mitochondrial Regulation of Diabetic Kidney Disease.Frontiers in medicine · 2021Review
- Sodium-Glucose Co-Transporter 2 Inhibitors Correct Metabolic Maladaptation of Proximal Tubular Epithelial Cells in High-Glucose Conditions.International journal of molecular sciences · 2020Article
- Kidney-based in vivo model for drug-induced nephrotoxicity testing.Scientific reports · 2020Article
- Modulation of Renal Injury by Variable Expression of Myo-Inositol Oxygenase (MIOX) via Perturbation in Metabolic Sensors.Biomedicines · 2020Article
- Article
- Inositols and metabolic disorders: From farm to bedside.Journal of traditional and complementary medicine · 2020Review
- Myo-inositol: its metabolism and potential implications for poultry nutrition-a review.Poultry science · 2020Review
- Autophagy Function and Regulation in Kidney Disease.Biomolecules · 2020Review
- Myo-inositol oxygenase expression profile modulates pathogenic ferroptosis in the renal proximal tubule.The Journal of clinical investigation · 2019Article
- Myo-inositol oxygenase accentuates renal tubular injury initiated by endoplasmic reticulum stress.American journal of physiology. Renal physiology · 2019Article
- Contribution of myo-inositol oxygenase in AGE:RAGE-mediated renal tubulointerstitial injury in the context of diabetic nephropathy.American journal of physiology. Renal physiology · 2018Article
- Nutritional and Acquired Deficiencies in Inositol Bioavailability. Correlations with Metabolic Disorders.International journal of molecular sciences · 2017Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Biological properties of renal-specific oxidoreductase (RSOR), characteristics of its promoter, and underlying mechanisms regulating its expression in diabetes were analyzed. RSOR expression, normally confined to the renal cortex, was markedly increased and extended into the outer medullary tubules in db/db mice, a model of type 2 diabetes. Exposure of LLCPK cells to d-glucose resulted in a dose-dependent increase in RSOR expression and its enzymatic activity. The latter was related to one of the glycolytic enzymes, myo-inositol oxygenase. The increase in activity was in proportion to serum glucose concentration. The RSOR expression also increased in cells treated with various organic osmolytes, e.g., sorbitol, myoinositol, and glycerolphosphoryl-choline and H(2)O(2). Basal promoter activity was confined to -1,252 bp upstream of ATG, and it increased with the treatment of high glucose and osmolytes. EMSAs indicated an increased binding activity with osmotic-, carbohydrate-, and oxidant-response elements in cells treated with high glucose and was abolished by competitors. Supershifts, detected by anti-nuclear factor of activated T cells, and carbohydrate-response-element-binding protein established the binding specificity. Nuclear factor of activated T cells tonicity-enhancer-binding protein and carbohydrate-response-element-binding protein had increased nuclear expression in cells treated with high glucose. The activity of osmotic-response element exhibited a unique alternate binding pattern, as yet unreported in osmoregulatory genes. Data indicate that RSOR activity is modulated by diverse mechanisms, and it is endowed with dual properties to channel glucose intermediaries, characteristic of hepatic aldehyde reductases, and to maintain osmoregulation, a function of renal medullary genes, e.g., aldose reductase, in diabetes.
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