Evidence map›Paper›PMID 35454131›Full record

ReviewBiomolecules2022

Advanced Glycation End Products and Diabetes Mellitus: Mechanisms and Perspectives.

Mariyam Khalid, Georg Petroianu, Abdu Adem

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 453 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
453citing papers in PubMed, 5 pooled it
91.9field-weighted citation impact, top 1% of its field
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

453 citing papers in PubMed, 5 syntheses or guidelines pooled it, 750 citations in OpenAlex.

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  19. Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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393 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Mariyam KhalidDepartment of Pharmacology and Therapeutics, College of Medicine and Health Sciences, Khalifa University, Abu Dhabi P.O. Box 127788, United Arab Emirates.ORCID 0000-0002-0327-0802
Georg PetroianuDepartment of Pharmacology and Therapeutics, College of Medicine and Health Sciences, Khalifa University, Abu Dhabi P.O. Box 127788, United Arab Emirates.ORCID 0000-0001-9110-4750
Abdu AdemDepartment of Pharmacology and Therapeutics, College of Medicine and Health Sciences, Khalifa University, Abu Dhabi P.O. Box 127788, United Arab Emirates.ORCID 0000-0002-9289-5301
Khalifa University of Science and Technology · AE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent hyperglycemic state in type 2 diabetes mellitus leads to the initiation and progression of non-enzymatic glycation reaction with proteins and lipids and nucleic acids. Glycation reaction leads to the generation of a heterogeneous group of chemical moieties known as advanced glycated end products (AGEs), which play a central role in the pathophysiology of diabetic complications. The engagement of AGEs with its chief cellular receptor, RAGE, activates a myriad of signaling pathways such as MAPK/ERK, TGF-β, JNK, and NF-κB, leading to enhanced oxidative stress and inflammation. The downstream consequences of the AGEs/RAGE axis involve compromised insulin signaling, perturbation of metabolic homeostasis, RAGE-induced pancreatic beta cell toxicity, and epigenetic modifications. The AGEs/RAGE signaling instigated modulation of gene transcription is profoundly associated with the progression of type 2 diabetes mellitus and pathogenesis of diabetic complications. In this review, we will summarize the exogenous and endogenous sources of AGEs, their role in metabolic dysfunction, and current understandings of AGEs/RAGE signaling cascade. The focus of this review is to recapitulate the role of the AGEs/RAGE axis in the pathogenesis of type 2 diabetes mellitus and its associated complications. Furthermore, we present an overview of future perspectives to offer new therapeutic interventions to intervene with the AGEs/RAGE signaling pathway and to slow down the progression of diabetes-related complications.

Indexed as

Diabetes ComplicationsDiabetes Mellitus, Type 2Glycation End Products, AdvancedHumansNF-kappa BOxidative StressReceptor for Advanced Glycation End ProductsGlycation End Products, AdvancedNF-kappa BReceptor for Advanced Glycation End Productsadvanced glycation end products (AGEs)diabetic complicationshyperglycemiapancreatic beta cellsreceptor for advanced glycation end products (RAGE)type 2 diabetes mellitus

Identifiers

PMID35454131
PMCPMC9030615
OpenAlexW4224307827

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.