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Proc Natl Acad Sci U S A. 2000 Mar 14;97(6):2809-13.

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

Author information

1
University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark, NJ 07103, USA.

Erratum in

  • Proc Natl Acad Sci U S A 2000 May 9;97(10):5679.

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

PMID:
10706607
PMCID:
PMC16011
DOI:
10.1073/pnas.040558497
[Indexed for MEDLINE]
Free PMC Article

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