TY - JOUR
T1 - Advanced glycation end product cross-linking
T2 - pathophysiologic role and therapeutic target in cardiovascular disease.
AU - Zieman, Susan
AU - Kass, David
N1 - Copyright:
This record is sourced from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
PY - 2004
Y1 - 2004
N2 - 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.
AB - 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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U2 - 10.1111/j.1527-5299.2004.03223.x
DO - 10.1111/j.1527-5299.2004.03223.x
M3 - Review article
C2 - 15184729
AN - SCOPUS:4344632810
SN - 1527-5299
VL - 10
SP - 144-149; quiz 150-151
JO - Congestive heart failure (Greenwich, Conn.)
JF - Congestive heart failure (Greenwich, Conn.)
IS - 3
ER -