ReviewGlycoconjugate journal2022
Advanced Glycation End Products: key player of the pathogenesis of atherosclerosis.
Review in Glycoconjugate journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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
33 citing papers in PubMed, 50 citations in OpenAlex.
- Modulation of circulating levels of advanced glycation end products and its impact on intima-media thickness of both common carotid arteries: CORDIOPREV randomised controlled trial.Cardiovascular diabetology · 2024Trial
- Article
- Association of novel lipid markers with cardiovascular and cerebrovascular disease risk: A cross-sectional NHANES 1999 to 2018 study.Medicine · 2026Article
- Article
- Cellular and Molecular Mechanisms of Hyperglycemia-Induced Atherosclerosis and Intervention Strategies of Chinese Herbal Medicine.Drug design, development and therapy · 2026Review
- AGE-RAGE Axis and Cardiovascular Diseases: Pathophysiologic Mechanisms and Prospects for Clinical Applications.Cardiovascular drugs and therapy · 2025Review
- Advanced glycation end products (AGEs) and their role in diabetes mellitus and related complications: mechanisms and therapeutic insights.Glycoconjugate journal · 2025Review
- Network pharmacology-based study in polymetformin's new function of blocking ages/rage pathway curing diabetic complications.Scientific reports · 2025Article
- Dihydromyricetin May Attenuate Skin Aging as a RAGE Inhibitor.Nutrients · 2025Article
- RAGE deficiency ameliorates abdominal aortic aneurysm progression.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- The Advanced Glycation End-Products (AGE)-Receptor for AGE System (RAGE): An Inflammatory Pathway Linking Obesity and Cardiovascular Diseases.International journal of molecular sciences · 2025Review
- The Peripheral Amyloid-β Nexus: Connecting Alzheimer's Disease with Atherosclerosis through Shared Pathophysiological Mechanisms.Neuromolecular medicine · 2025Review
- Association between glycation gap and impaired cardiorespiratory fitness: evidence from American adults.BMC cardiovascular disorders · 2025Article
- Methylglyoxal Formation-Metabolic Routes and Consequences.Antioxidants (Basel, Switzerland) · 2025Review
- The Role of Advanced Glycation End Products in Saphenous Vein Graft Failure.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2025Article
- Mesenchymal stem cell therapy in atherosclerosis: A bibliometric and visual analysis.World journal of stem cells · 2024Article
- Glycated Hemoglobin and Cardiovascular Disease in Patients Without Diabetes.Journal of clinical medicine · 2024Review
- Diabetic Glycation of Human Serum Albumin Affects Its Immunogenicity.Biomolecules · 2024Article
- Usefulness of Serum Testosterone Concentration and Skin Autofluorescence as Coronary Risk Markers in Male Patients With Type 2 Diabetes Mellitus.Cardiology research · 2024Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis is the most common type of cardiovascular disease, and it causes intima thickening, plaque development, and ultimate blockage of the artery lumen. Advanced glycation end products (AGEs) are thought to have a role in the development and progression of atherosclerosis. there is developing an enthusiasm for AGEs as a potential remedial target. AGES mainly induce arterial damage and exacerbate the development of atherosclerotic plaques by triggering cell receptor-dependent signalling. The interplay of AGEs with RAGE, a transmembrane signalling receptor present across all cells important to atherosclerosis, changes cell activity, boosts expression of genes, and increases the outflow of inflammatory compounds, resulting in arterial wall injury and plaque formation. Here in this review, function of AGEs in the genesis, progression, and instability of atherosclerosis is discussed. In endothelial and smooth muscle cells, as well as platelets, the interaction of AGEs with their transmembrane cell receptor, RAGE, triggers intracellular signalling, resulting in endothelial damage, vascular smooth muscle cell function modification, and changed platelet activity.
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What OpenQuestion 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 OpenQuestion graph.