Advanced glycation end product cross-linking

pathophysiologic role and therapeutic target in cardiovascular disease.

Susan Zieman, David A Kass

Research output: Contribution to journalArticle

Abstract

Advanced glycation end products (AGEs) form by a nonenzymatic reaction between reducing sugars and biological proteins. These stable compounds accumulate slowly throughout the life span and contribute to structural and physiologic changes in the cardiovascular system such as increased vascular and myocardial stiffness, endothelial dysfunction, altered vascular injury responses, and atherosclerotic plaque formation. Mechanisms underlying these alterations include AGE cross-linking of collagen and AGE interactions with circulating proteins and AGE receptors. The clinical manifestations of AGE accrual-isolated systolic hypertension, endothelial and diastolic dysfunction, and atherosclerosis-underscore their role in increased cardiovascular risk associated with aging as well as diabetes and hypertension, conditions that enhance AGE formation. New pharmacologic agents that prevent AGE, break cross-links, or block AGE receptors reduce vascular and myocardial stiffness, inhibit atherosclerotic plaque formation, and improve endothelial function. These agents promise to reduce the risk of isolated systolic hypertension, diastolic dysfunction, and diabetes, and thus, heart failure.

Original languageEnglish (US)
JournalCongestive heart failure (Greenwich, Conn.)
Volume10
Issue number3
StatePublished - May 2004

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Advanced Glycosylation End Products
Vascular Stiffness
Cardiovascular Diseases
Atherosclerotic Plaques
Hypertension
Vascular System Injuries
Cardiovascular System
Atherosclerosis
Proteins
Collagen
Therapeutics
Heart Failure
Advanced Glycosylation End Product-Specific Receptor

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

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abstract = "Advanced glycation end products (AGEs) form by a nonenzymatic reaction between reducing sugars and biological proteins. These stable compounds accumulate slowly throughout the life span and contribute to structural and physiologic changes in the cardiovascular system such as increased vascular and myocardial stiffness, endothelial dysfunction, altered vascular injury responses, and atherosclerotic plaque formation. Mechanisms underlying these alterations include AGE cross-linking of collagen and AGE interactions with circulating proteins and AGE receptors. The clinical manifestations of AGE accrual-isolated systolic hypertension, endothelial and diastolic dysfunction, and atherosclerosis-underscore their role in increased cardiovascular risk associated with aging as well as diabetes and hypertension, conditions that enhance AGE formation. New pharmacologic agents that prevent AGE, break cross-links, or block AGE receptors reduce vascular and myocardial stiffness, inhibit atherosclerotic plaque formation, and improve endothelial function. These agents promise to reduce the risk of isolated systolic hypertension, diastolic dysfunction, and diabetes, and thus, heart failure.",
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