ReviewAntioxidants (Basel, Switzerland)2025
Role of Advanced Glycation End Products and Mitohormesis in Cancer Development and Progression.
Review in Antioxidants (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Serum-Soluble Receptor for Advanced Glycation End Products as a Potential Biomarker in Lung Cancer Patients.Journal of personalized medicine · 2026Article
- Balancing the dual nature of glycotoxins: interplay of diet, digestion, and gut microbiome.Frontiers in nutrition · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Advanced glycation end products (AGEs) are molecules formed via non-enzymatic reactions between reactive dicarbonyls and macromolecules, including proteins, lipids, or DNA. Mitochondria sense and integrate stress signals and induce changes in cellular function by regulating metabolism, redox balance, and proteostasis to maintain homeostasis, a process known as mitohormesis. Dysregulation of cellular metabolism and redox imbalance are the major driving forces behind the increased production of intracellular reactive dicarbonyls and AGEs. Although the association between increased reactive dicarbonyl levels and cancer development has been investigated, its causal relationship remains controversial. This review integrates recent evidence on the association between increased levels of reactive dicarbonyls and mitochondrial dysfunction and provides mechanistic insights into carcinogenesis associated with AGE-mediated disruption of mitohormesis.
Indexed as
Identifiers
What 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.