ReviewMolecular biology reports2025
Molecular pathways of oxidative stress in diabetes: redox imbalance and insulin pathway dysregulation.
Review in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Oxidative Stress Biomarkers in Pediatric and Early-Stage Type 1 Diabetes: Toward Redox Phenotyping.Antioxidants (Basel, Switzerland) · 2026Review
- Oxidative Stress in Diabetic Cardiomyopathy: Molecular Mechanisms and Emerging Therapeutic Targets.Biomolecules · 2026Review
- Elucidating the Effects of Selenium Enrichment on the Structure and Antioxidant Properties of Selenium-Containing Proteins in Yeast Cells.Antioxidants (Basel, Switzerland) · 2026Article
- Running out the clock: Circadian rhythm dysfunction in cognitive disease.International review of neurobiology · 2026Review
- A putativeFrontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress plays a pivotal role in the pathogenesis of diabetes mellitus, primarily triggered by hyperglycaemia-induced activation of various metabolic pathways such as glycolytic, hexosamine, PKC, polyol, and AGE pathways. A critical event in this process is the inhibition of GAPDH mediated by PARP-1, leading to the accumulation of glyceraldehyde-3-phosphate, which subsequently promotes the formation of AGE through methylglyoxal, augments PKC signalling, and enhances flux through the polyol and hexosamine pathways. This oxidative imbalance disrupts the IRS-PI3K-GLUT signalling axis, resulting in diminished glucose uptake and contributing to systemic insulin resistance and β-cell damage. Genetic and epigenetic variations, coupled with compromised antioxidant defences, exacerbate susceptibility to oxidative stress, while the Keap1-Nrf2-ARE pathway emerges as a crucial mechanism for reinstating redox equilibrium.
Indexed as
Identifiers
41460371What Socratic holds
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 Socratic graph.