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, an
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 (≈40%) in age-related left ventricular
stiffness was observed [(57.1 ± 6.8
mmHg⋅m
2
/ml pretreatment and 33.1 ± 4.6
mmHg⋅m
2
/ml posttreatment (1 mmHg = 133 Pa)].
This decrease was accompanied by improvement in cardiac function.
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