ReviewThe International journal of angiology : official publication of the International College of Angiology, Inc2015
Role of Advanced Glycation End Products and Its Receptors in the Pathogenesis of Cigarette Smoke-Induced Cardiovascular Disease.
Review in The International journal of angiology : official publication of the International College of Angiology, Inc, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 82 citations in OpenAlex.
- Review
- The Role of Advanced Glycation End-Products in the Pathophysiology and Pharmacotherapy of Cardiovascular Disease.International journal of molecular sciences · 2025Review
- Assessment and prediction models for the quantitative and qualitative reserve of the ovary using machine learning.Journal of ovarian research · 2025Article
- Article
- The dual challenge of diabesity: pathophysiology, management, and future directions.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Relationship Between Advanced Glycation End Products Tissue Accumulation and Frailty in Patients Undergoing Cardiac Rehabilitation.Cardiology research · 2025Article
- Effects of Advanced Glycation End Products (AGEs) on Human Lung Macrophages: Implications for Pulmonary Inflammation.Journal of inflammation research · 2025Article
- Cardiovascular risks and endothelial dysfunction in reproductive-age women with endometriosis.Scientific reports · 2024Article
- Serum Advanced Glycation End Products and Their Soluble Receptor as New Biomarkers in Systemic Lupus Erythematosus.Biomedicines · 2024Article
- The RAGE/DIAPH1 axis: mediator of obesity and proposed biomarker of human cardiometabolic disease.Cardiovascular research · 2024Review
- Protein Advanced Glycation End Products and Their Implications in Pancreatic Cancer.Cancer prevention research (Philadelphia, Pa.) · 2023Review
- Article
- Implications of receptor for advanced glycation end products for progression from obesity to diabetes and from diabetes to cancer.World journal of diabetes · 2023Review
- Signaling pathways in vascular function and hypertension: molecular mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2023Review
- Accelerated AGEing: The Impact of Advanced Glycation End Products on the Prognosis of Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Role of the renin-angiotensin system in the pathophysiology of coronary heart disease and heart failure: Diagnostic biomarkers and therapy with drugs and natural products.Frontiers in physiology · 2023Review
- Roles of endoplasmic reticulum stress in the pathophysiology of polycystic ovary syndrome.Frontiers in endocrinology · 2023Review
- Article
- Advanced Glycation End Products (AGEs) and Chronic Kidney Disease: Does the Modern Diet AGE the Kidney?Nutrients · 2022Review
- Mechanism of Hypercholesterolemia-Induced Atherosclerosis.Reviews in cardiovascular medicine · 2022Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The interaction of advanced glycation end products (AGEs) with its cell-bound receptor RAGE increases gene expression and release of proinflammatory cytokines and increase generation of reactive oxygen species (ROS). Circulating receptors, soluble RAGE (sRAGE), and endosecretory RAGE (esRAGE) by binding with RAGE ligands have protective effects against AGE-RAGE interaction. Cigarette smoking is a risk factor for coronary artery disease, stroke, and peripheral vascular disease. This article reviews; if the AGE-RAGE axis is involved in the cigarette smoke-induced cardiovascular diseases. There are various sources of AGEs in smokers including, gas/tar of cigarette, activation of macrophages and polymorphonuclear leukocytes, uncoupling of endothelial isoform of nitric oxide synthase (eNOS) and xanthine oxidase. The levels of AGEs are elevated in smokers. Serum levels of sRAGE have been reported to be reduced, elevated, or unchanged in smokers. Mostly the levels are reduced. There is one article which shows an elevation of levels of sRAGE in smokers. Serum levels of esRAGE are unaltered in smokers. Mechanism of AGE-RAGE-induced atherosclerosis has been discussed. Atherosclerosis leads to the cardiovascular diseases. It has been suggested that ratio of AGE/sRAGE or AGE/esRAGE is useful in determining the deleterious effects of AGE-RAGE interaction in smokers. sRAGE alone is not a good marker for smoke-induced cardiovascular disease. In conclusion cigarette smoke induces formation of AGEs and reduces sRAGE resulting in the development of atherosclerosis and related coronary heart disease, stroke, and peripheral vascular disease. Ratio of AGEs/sRAGE is a better marker for cardiovascular disease than AGEs or sRAGE alone in smokers.
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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.