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Cardiovascular Research 2000 46(2):239-249; doi:10.1016/S0008-6363(00)00043-2
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Matrix gene expression and decompensated heart failure

The aged SHR model

Marvin O. Boluyta,* and Oscar H.L. Bingb

aThe University of Michigan, Laboratory of Molecular Kinesiology, 401 Washtenaw Avenue, Ann Arbor, MI 48109-2214, USA
bThe Department of Medicine, Boston Veterans Affairs Medical Center, Boston, MA 02130, USA

* Corresponding author. Tel.: +1-313-647-7645; fax: +1-313-936-1925 boluytm{at}umich.edu

Impaired functional performance despite hypertrophic enlargement, and an excessive accumulation of extracellular matrix, are hallmarks of the decompensated failing heart. Age is the leading risk factor for heart failure, and there is evidence suggesting that a number of age-associated changes in the cardiac phenotype predispose the heart to failure. The spontaneously hypertensive rat (SHR) exhibits compensated cardiac hypertrophy followed by a transition to heart failure in the last quartile of the lifespan, and thus provides a useful model of the transition from stable compensated hypertrophy to decompensated heart failure in the context of aging. The transition to failure in the SHR is accompanied by marked changes in the expression of an array of genes in the heart, including increased expression of a number of genes associated with the extracellular matrix. Drug treatments that prevent or reverse matrix gene expression in the SHR heart improve myocardial function and survival. The aged SHR model of decompensated heart failure has provided insight into the role of the extracellular matrix in the transition to failure, and can be useful to further investigate the mechanistic bases of heart failure, as well as to evaluate the potential efficacy of novel therapeutic approaches to the treatment of heart failure.

KEYWORDS Aging; Extracellular matrix; Fibrosis; Heart failure; Hypertension


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