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An advanced glycation endproduct cross-link breaker can reverse age-related increases in myocardial stiffness 

Asif, M., Egan, J., Vasan, S., Jyothirmayi, G. N., Masurekar, M. R., Lopez, S., Williams, C., Torres, R. L., Wagle, D., Ulrich, P. 

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Abstract
Decreased elasticity of the cardiovascular system is one of the hallmarks of the normal aging process of mammals. A potential explanation for this decreased elasticity is that glucose can react nonenzymatically with long-lived proteins, such as collagen and lens crystallin, and link them together, producing advanced glycation endproducts (AGEs). Previous studies have shown that aminoguanidine, and AGE inhibitor, can prevent glucose cross-linking of proteins and the loss of elasticity associated with aging and diabetes. Recently, an AGE cross-link breaker (ALT-711) has been described, which we have evaluated in aged dogs. After 1 month of administration of ALT-711, a significant reduction (apprxeq40%) in age-related left ventricular stiffness was observed ((57.1 +- 6.8 mmHgcntdotm2/ml pretreatment and 33.1 +- 4.6 mmHgcntdotm2/ml posttreatment (1 mmHg = 133 Pa)). This decrease was accompanied by improvement in cardiac function.

Reference

PNAS: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA ,   97(6):2809-2813 2000     

 

Updated January 2016

 

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