ReviewJournal of diabetes research2014
Pathogenesis of chronic hyperglycemia: from reductive stress to oxidative stress.
Review in Journal of diabetes research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 202 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
202 citing papers in PubMed, 1 synthesis or guideline pooled it, 387 citations in OpenAlex.
- Potential Effects of Sweet Potato (International journal of molecular sciences · 2021Pooled it
- Trial
- TNFOxidative medicine and cellular longevity · 2020Trial
- Relationship Between Hypovitaminosis C, Obesity, and Features of Metabolic Syndrome-A Narrative Review.Nutrition reviews · 2026Review
- The Reductive Stress Nexus: Integrated Pathways of Metabolic Dysregulation, Senescence and Blood-Brain Barrier Failure in Neurodegenerative Disease and Brain Aging.Cell biochemistry and biophysics · 2026Review
- Bacopa monniera: A Promising Phytotherapeutic Approach in Management of Diabetes-Related Complications.Phytotherapy research : PTR · 2026Review
- Multidimensional Unraveling Insights from an Enzyme-Nanozyme Cascade-Based Electrochemical Biosensor for Screening Microplastic Neurotoxicity.Environment & health (Washington, D.C.) · 2026Article
- Tuning the Fire: Context-Dependent Mitochondrial ROS Signaling, Mitohormesis, and Redox-Modulating Interventions.Biomolecules · 2026Review
- Article
- Over-Intake of Plant-Derived Antioxidants, HInternational journal of molecular sciences · 2026Article
- Docosahexaenoic acid is comparable to vildagliptin in improving hyperglycemia and pancreatic insulin signaling of diabetic rats via SIRT1/Akt/PI3K pathway.Scientific reports · 2026Article
- Mitochondrial mGPDH Modulates Fibroblast Function in Diabetic Wound Healing via the SIRT1-c-Myc-TGF-β1 Axis.Diabetes · 2026Article
- Sustained cadmium exposure and hyperglycemia additively drives mitochondrial dysfunction in hepatic cells: Implications for MASLD etiopathogenesis.Toxicology and applied pharmacology · 2026Article
- Diabetes-induced Multiorgan Damage: Can Magnesium Delay the process?Current nutrition reports · 2026Review
- The Central Role of Oxidative Stress in Diabetic Retinopathy: Advances in Pathogenesis, Diagnosis, and Therapy.Diagnostics (Basel, Switzerland) · 2026Review
- Reductive stress in cancer immunology and targeted therapy.Acta biochimica et biophysica Sinica · 2026Review
- Role of Antioxidants in Diseases and its Impact on Mitochondria with A Focus on Diabetes: An Overview.Current drug research reviews · 2026Review
- Breathomics in Diabetes Management: A Noninvasive Approach for Precision Health Monitoring.Journal of diabetes research · 2026Review
- Long non-coding RNAs in the crosstalk between diabetes and colorectal cancer: molecular mechanisms and endocrine pathways.Frontiers in molecular biosciences · 2026Review
- Molecular pathways of oxidative stress in diabetes: redox imbalance and insulin pathway dysregulation.Molecular biology reports · 2025Review
142 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Chronic overnutrition creates chronic hyperglycemia that can gradually induce insulin resistance and insulin secretion impairment. These disorders, if not intervened, will eventually be followed by appearance of frank diabetes. The mechanisms of this chronic pathogenic process are complex but have been suggested to involve production of reactive oxygen species (ROS) and oxidative stress. In this review, I highlight evidence that reductive stress imposed by overflux of NADH through the mitochondrial electron transport chain is the source of oxidative stress, which is based on establishments that more NADH recycling by mitochondrial complex I leads to more electron leakage and thus more ROS production. The elevated levels of both NADH and ROS can inhibit and inactivate glyceraldehyde 3-phosphate dehydrogenase (GAPDH), respectively, resulting in blockage of the glycolytic pathway and accumulation of glycerol 3-phospate and its prior metabolites along the pathway. This accumulation then initiates all those alternative glucose metabolic pathways such as the polyol pathway and the advanced glycation pathways that otherwise are minor and insignificant under euglycemic conditions. Importantly, all these alternative pathways lead to ROS production, thus aggravating cellular oxidative stress. Therefore, reductive stress followed by oxidative stress comprises a major mechanism of hyperglycemia-induced metabolic syndrome.
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Registered trials
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.