Evidence map›Paper›PMID 40474023›Full record

ReviewMolecular biology reports2025

Mechanism and implications of advanced glycation end products (AGE) and its receptor RAGE axis as crucial mediators linking inflammation and obesity.

Sajani Arunkumar Kavitha, Sara Zainab, Yadav Sangeeta Muthyalaiah, Cordelia Mano John, Sumathy Arockiasamy

Abstract readReview
PubMed Publisher
In one paragraph

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 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed.

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  8. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
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  17. Djulis (Molecules (Basel, Switzerland) · 2025
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Sajani Arunkumar KavithaDepartment of Biomedical Sciences, Sri Ramachandra Institute of Higher Education and Research, Porur, Chennai, India, 600116.
Sara ZainabDepartment of Biomedical Sciences, Sri Ramachandra Institute of Higher Education and Research, Porur, Chennai, India, 600116.
Yadav Sangeeta MuthyalaiahDepartment of Biomedical Sciences, Sri Ramachandra Institute of Higher Education and Research, Porur, Chennai, India, 600116.
Cordelia Mano JohnDepartment of Biomedical Sciences, Sri Ramachandra Institute of Higher Education and Research, Porur, Chennai, India, 600116.
Sumathy ArockiasamyDepartment of Biomedical Sciences, Sri Ramachandra Institute of Higher Education and Research, Porur, Chennai, India, 600116. sumathyjoseph04@sriramachandra.edu.in.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Advanced glycation end products (AGEs) are heterogenous compounds that play a central role in various chronic diseases, such as diabetes, neurodegenerative disorders, cardiovascular diseases, and cancer. These are formed by non-enzymatic reaction between reducing sugar and amino group of proteins, lipids and nucleic acids. Elevated levels of AGEs are associated with obesity, which is linked to hyperglycemia, dyslipidemia and insulin resistance, contributing to metabolic syndrome and diabetes. Both dietary and endogenous AGEs contribute to persistent oxidative stress and inflammation directly through glycated biomolecules and indirectly through its receptor, receptor for advanced glycation end products, RAGE. In this context, inflammation is a sustained, systemic immune response with macrophage infiltration into adipose tissues, high pro- inflammatory cytokines leading to immune dysregulation, activation of key inflammatory pathways such as NF-kB and JNK signaling, increase oxidative stress, insulin resistance suggesting inflammation as both a cause and consequence of metabolic dysfunction. Persistent oxidative stress and inflammation accelerates AGEs formation, disrupt cellular signaling, alter extracellular matrix integrity, impair release of enzymes and hormones. Also, AGE-induced gut microbiome imbalance elicits conditions such as systemic inflammation, intestinal barrier dysfunction and metabolic imbalance, promoting obesity and its complications. This review explores the central role of AGEs in obesity-associated inflammation, emphasizing AGE-RAGE signaling, epigenetic regulation and gut microbiome dysfunction. Understanding this interplay mediated by AGEs is critical for identifying potential biomarkers of metabolic risk and strategize means to prevent AGEs formation, block AGE-RAGE interaction and signaling, thus mitigating the effects of obesity and its associated diseases.

Indexed as

Glycation End Products, AdvancedInflammationObesityReceptor for Advanced Glycation End ProductsAnimalsEpigenesis, GeneticGastrointestinal MicrobiomeHumansInsulin ResistanceMetabolic SyndromeOxidative StressSignal TransductionGlycation End Products, AdvancedReceptor for Advanced Glycation End ProductsAdvanced glycation end products (AGEs)InflammationMetabolic syndromeObesityReceptor for advanced glycation end products RAGE

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.