Abstract
Atherosclerosis is the main contributor to cardiovascular disease and leads to intimal plaque formation, which may progress to plaque rupture with subsequent thromboembolic events and/or occlusion of the arterial lumen. There is increasing evidence that the development or progression of atherosclerosis is associated with advanced glycation endproducts (AGEs). AGEs are a heterogeneous group of compounds formed by the non-enzymatic reaction of reducing sugars with proteins, lipids, and nucleic acids. An increased understanding of the mechanisms of formation and interaction of AGEs has allowed the development of several potential anti-AGE strategies. This review summarizes AGE formation and biochemistry, the pathogeneic role of AGEs in cardiovascular disease, anti-AGE therapies and clinical relevance to vascular surgery.
MeSH terms
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Atherosclerosis / complications
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Atherosclerosis / metabolism*
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Atherosclerosis / physiopathology
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Atherosclerosis / surgery
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Biomarkers / metabolism
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Blood Vessel Prosthesis
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Blood Vessel Prosthesis Implantation / instrumentation
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Cardiovascular Diseases / etiology*
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Cardiovascular Diseases / metabolism
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Cardiovascular Diseases / prevention & control
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Diabetic Foot / metabolism*
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Diabetic Foot / physiopathology
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Diabetic Foot / surgery
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Disease Progression
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Glycation End Products, Advanced / antagonists & inhibitors
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Glycation End Products, Advanced / metabolism*
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Graft Occlusion, Vascular / etiology
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Graft Occlusion, Vascular / metabolism
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Humans
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Stents
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Treatment Outcome
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Vascular Patency
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Vascular Surgical Procedures* / adverse effects
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Vascular Surgical Procedures* / instrumentation
Substances
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Biomarkers
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Glycation End Products, Advanced