ReviewMolecular biology reports2025
The mechanistic interplay of reactive oxygen species in metabolic pathways and insulin signaling in type 2 diabetes.
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 1 paper.
What it found
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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
1 citing paper in PubMed.
- Osteoarthritis and dementia: contrasting disorders driven by mutual pathways of autophagy, mTOR, GLP-1, AMPK, Wnt, and WISP1.Expert review of clinical pharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes mellitus is a chronic disorder marked by elevated blood sugar due to insufficient insulin production, reduced insulin sensitivity, or both. The global incidence of diabetes has four-fold the past 20 years, creating a significant health crisis. According to the International Diabetes Federation (2025), around 589 million adults aged 20 to 79 were living with diabetes in 2024. Among this group, more than 9.5 million were affected by type 1 diabetes, including approximately 1.9 million children and adolescents below 20 years of age. By 2050, the global number of individuals with diabetes is anticipated to increase to nearly 853 million. It is classified into type 1 (DM1), which destroys pancreatic β-cells, and type 2 (DM2), primarily linked to insulin resistance. Persistent hyperglycemia in DM causes organ damage, leading to both microvascular and macrovascular complications. OS is crucial in DM’s onset and progression. ROS produced during oxygen metabolism, disrupt cellular metabolic processes and cause oxidative damage. This imbalance between ROS production and antioxidant defences worsens DM complications by impairing insulin production and action. In DM1, ROS reduce β-cell functionality, and hyperglycemia further induces oxidative stress. Key molecular pathways involved in oxidative stress during DM are glycolysis, the hexosamine pathway, PKC activation, and the polyol pathway. Hyperglycemia-induced mitochondrial superoxide inhibits GAPDH, causing glyceraldehyde-3-phosphate to accumulate and activate pro-oxidative pathways. AGEs enhance ROS production, further contributing to oxidative stress. Elevated glucose levels also activate the hexosamine pathway, leading to toxic effects and DM complications. In conclusion, OS plays a major role in DM development and complications, though antioxidant interventions have shown limited preventive effects. Understanding oxidative mechanisms in DM can guide future therapeutic strategies.
Indexed as
Identifiers
41240140What 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.