Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Higher levels of advanced glycation endproducts in human carotid atherosclerotic plaques are associated with a rupture-prone phenotype.

European heart journal - 1 May 2014

Hanssen Nordin M J, Wouters Kristiaan, Huijberts Maya S, Gijbels Marion J, Sluimer Judith C, Scheijen Jean L J M, Heeneman Sylvia, Biessen Erik A L, Daemen Mat J A P, Brownlee Michael, de Kleijn Dominique P, Stehouwer Coen D A, Pasterkamp Gerard, Schalkwijk Casper G

Abstract excerpt

AIMS: Rupture-prone atherosclerotic plaques are characterized by inflammation and a large necrotic core. Inflammation is linked to high metabolic activity. Advanced glycation endproducts (AGEs) and their major precursor methylglyoxal are formed during high metabolic activity and can have detrimental effects on cellular function and may induce cell death. Therefore, we investigated whether plaque AGEs are...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Apoptosis
Share to Carotid Artery Diseases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Hypoxia

Share to Glycation End Products, Advanced

Share to Leukocytes, Mononuclear

Share to Macrophages

Share to Plaque, Atherosclerotic

Share to Tumor Necrosis Factor-alpha

Source

Identifiers

PMID: 24126878
DOI: 10.1093/eurheartj/eht402

Genes

TNF

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Higher levels of advanced glycation endproducts in human carotid atherosclerotic plaques are associated with a rupture-prone phenotype.PMID 24126878Read ↗

Methylglyoxal in Cardiometabolic Disorders – Routes Leading to Pathology – Counterbalanced by Treatment StrategiesSemantic proximity Read ↗

N-Terminal proteomics reveals distinct protein degradation patterns in different types of human atherosclerotic plaquesSemantic proximity Read ↗

Methylglyoxal-derived advanced glycation end products contribute to negative cardiac remodeling and dysfunction post-myocardial infarction.Semantic proximity Read ↗

Discovery of Diagnostic and Therapeutic Targets For Vascular Injury Induced By Methylglyoxal Using ProteomicsSemantic proximity Read ↗

Status of biomarkers for the identification of stable or vulnerable plaques in atherosclerosis.Semantic proximity Read ↗

Hyaluronic acid metabolism is increased in unstable plaques.Semantic proximity Read ↗

A Cyclic Arginine Adduct Eclipses Carboxymethylation as the Primary Glyoxal-Derived Advanced Glycation End-ProductSemantic proximity Read ↗

Genome-scale metabolic network of human carotid plaque reveals the pivotal role of glutamine/glutamate metabolism in macrophage modulating plaque inflammation and vulnerability.Semantic proximity Read ↗

Methylglyoxal Potentiates Palmitic Acid-Induced Endothelial Dysfunction and Atherogenesis in HUVECsSemantic proximity Read ↗

Atherosclerotic Plaque Fissuration and Clinical Outcomes in Pre-Diabetics vs. Normoglycemics Patients Affected by Asymptomatic Significant Carotid Artery Stenosis at 2 Years of Follow-Up: Role of MIcRoRNAs Modulation. The ATIMIR StudySemantic proximity Read ↗

DNA methylation dynamics in human carotid plaques after cerebrovascular events.Semantic proximity Read ↗

DNA methylome profiling reveals epigenetic regulation of lipoprotein-associated phospholipase A2 in human vulnerable atherosclerotic plaque.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.