ArticleThe Journal of biological chemistry2016
myo-Inositol Oxygenase Overexpression Accentuates Generation of Reactive Oxygen Species and Exacerbates Cellular Injury following High Glucose Ambience: A NEW MECHANISM RELEVANT TO THE PATHOGENESIS OF DIABETIC NEPHROPATHY.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Long noncoding RNA NEAT1 promotes ferroptosis by modulating the miR-362-3p/MIOX axis as a ceRNA.Cell death and differentiation · 2022Article
- Effects of Bee Propolis on FBG, HbA1c, and Insulin Resistance in Healthy VolunteersTurkish journal of pharmaceutical sciences · 2021Article
- Comparing the renoprotective effects of the antioxidants melatonin, vitamin D and vitamin E in diabetic rats.Journal of Taibah University Medical Sciences · 2020Article
- Increased mitochondrial fission of glomerular podocytes in diabetic nephropathy.Endocrine connections · 2019Article
- Protective effects of curcumin on diabetic nephropathy via attenuation of kidney injury molecule 1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) expression and alleviation of oxidative stress in rats with type 1 diabetes.Iranian journal of basic medical sciences · 2019Article
- Myo-inositol oxygenase accentuates renal tubular injury initiated by endoplasmic reticulum stress.American journal of physiology. Renal physiology · 2019Article
- Huangqi decoction inhibits hyperglycemia-induced podocyte apoptosis by down-regulated Nox4/p53/Bax signalingAmerican journal of translational research · 2019Article
- Reactive oxygen species promote tubular injury in diabetic nephropathy: The role of the mitochondrial ros-txnip-nlrp3 biological axis.Redox biology · 2018Article
- Anthocyanins inhibit high glucose-induced renal tubular cell apoptosis caused by oxidative stress in db/db mice.International journal of molecular medicine · 2018Article
- Myo-inositol Oxygenase as a Novel Marker in the Diagnosis of Acute Kidney Injury.Journal of medical biochemistry · 2018Article
- 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
- Review
- Concise Review: Current and Emerging Biomarkers of Nephrotoxicity.Current opinion in toxicology · 2017Article
- Beneficial Effects ofJournal of the American Society of Nephrology : JASN · 2017Article
- High Glucose-Induced Hypomethylation Promotes Binding of Sp-1 to Myo-Inositol Oxygenase: Implication in the Pathobiology of Diabetic Tubulopathy.The American journal of pathology · 2017Article
- The mitochondria-targeted antioxidant MitoQ ameliorated tubular injury mediated by mitophagy in diabetic kidney disease via Nrf2/PINK1.Redox biology · 2017Article
- Serotonin and Its Receptor as a New Antioxidant Therapeutic Target for Diabetic Kidney Disease.Journal of diabetes research · 2017Review
- An update on diabetic kidney disease, oxidative stress and antioxidant agents.Journal of renal injury prevention · 2017Article
- Hydrogen-Rich Saline Promotes the Recovery of Renal Function after Ischemia/Reperfusion Injury in Rats via Anti-apoptosis and Anti-inflammation.Frontiers in pharmacology · 2016Article
- Inositols in Midlife.Journal of mid-life healthArticle
Corrections and comments
- Retraction · 2019-06-28Manipulation of Images ·
- RetractedWithdrawal:2019
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Diabetic nephropathy (DN) is characterized by perturbations in metabolic/cellular signaling pathways with generation of reactive oxygen species (ROS). The ROS are regarded as a common denominator of various pathways, and they inflict injury on renal glomerular cells. Recent studies indicate that tubular pathobiology also plays a role in the progression of DN. However, the mechanism(s) for how high (25 mm) glucose (HG) ambience induces tubular damage remains enigmatic. myo-Inositol oxygenase (MIOX) is a tubular enzyme that catabolizes myo-inositol to d-glucuronate via the glucuronate-xylulose (G-X) pathway. In this study, we demonstrated that G-X pathway enzymes are expressed in the kidney, and MIOX expression/bioactivity was up-regulated under HG ambience in LLC-PK1 cells, a tubular cell line. We further investigated whether MIOX overexpression leads to accentuation of tubulo-interstitial injury, as gauged by some of the parameters relevant to the progression of DN. Under HG ambience, MIOX overexpression accentuated redox imbalance, perturbed NAD(+)/NADH ratios, increased ROS generation, depleted reduced glutathione, reduced GSH/GSSG ratio, and enhanced adaptive changes in the profile of the antioxidant defense system. These changes were also accompanied by mitochondrial dysfunctions, DNA damage and induction of apoptosis, accentuated activity of profibrogenic cytokine, and expression of fibronectin, the latter two being the major hallmarks of DN. These perturbations were largely blocked by various ROS inhibitors (Mito Q, diphenyleneiodonium chloride, and N-acetylcysteine) and MIOX/NOX4 siRNA. In conclusion, this study highlights a novel mechanism where MIOX under HG ambience exacerbates renal injury during the progression of diabetic nephropathy following the generation of excessive ROS via an unexplored G-X pathway.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.