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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. Abstract
broadcast on www.provet.co.uk
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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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