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European Journal of Heart Failure 2007 9(12):1146-1155; doi:10.1016/j.ejheart.2007.09.009
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© 2007 European Society of Cardiology

Advanced glycation end-products (AGEs) and heart failure: Pathophysiology and clinical implications

Jasper W.L. Hartoga,*, Adriaan A. Voorsa, Stephan J.L. Bakkerb, Andries J. Smitb and Dirk J. van Veldhuisena

a Department of Cardiology, Thoraxcenter, University Medical Center Groningen and University of Groningen Hanzeplein 1, P.O. Box 30001, 9700 RB Groningen, The Netherlands
b Department of Medicine, University Medical Center Groningen and University of Groningen Hanzeplein 1, P.O. Box 30001, 9700 RB Groningen, The Netherlands

* Corresponding author. Tel.: +31 50 361 2355; fax: +31 50 361 4391. j.w.l.hartog{at}thorax.umcg.nl(J.W.L. Hartog).


  Abstract

Advanced glycation end-products (AGEs) are molecules formed during a non-enzymatic reaction between proteins and sugar residues, called the Maillard reaction. AGEs accumulate in the human body with age, and accumulation is accelerated in the presence of diabetes mellitus. In patients with diabetes, AGE accumulation is associated with the development of cardiac dysfunction. Enhanced AGE accumulation is not restricted to patients with diabetes, but can also occur in renal failure, enhanced states of oxidative stress, and by an increased intake of AGEs. Several lines of evidence suggest that AGEs are related to the development and progression of heart failure in non-diabetic patients as well. Preliminary small intervention studies with AGE cross-link breakers in heart failure patients have shown promising results. In this review, the role of AGEs in the development of heart failure and the role of AGE intervention as a possible treatment for heart failure are discussed.

Key Words: Heart failure • Advanced glycation end-products • Atherosclerosis • Oxidative stress • Cross-linking

Received April 19, 2007; Revised August 1, 2007; Accepted September 26, 2007


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