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Cardiovascular Research Advance Access first published online on December 1, 2008
This version [Corrected Proof] published online on December 23, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn337
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org.

Telomere biology in cardiovascular disease: the TERC–/– mouse as a model for heart failure and ageing

Liza S.M. Wong, Hisko Oeseburg, Rudolf A. de Boer, Wiek H. van Gilst, Dirk J. van Veldhuisen and Pim van der Harst*

Department of Cardiology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, 9700RB Groningen, The Netherlands

* Corresponding author. Tel: +31 50 3612355; fax: +31 50 3614391. E-mail address: P.van.der.Harst{at}thorax.umcg.nl

Atherosclerosis and heart failure are major causes of morbidity and mortality in Western countries. Recent studies are suggesting involvement of telomere biology in the development and progression of age-associated conditions, including hypertension, atherosclerosis, and heart failure. Whether any of these reported associations are based on causal relationships remains to be elucidated. The construction of telomerase-deficient (telomerase RNA component, TERC–/–) mice might provide a potential instrumental model to study the involvement of telomere biology in cardiovascular disease. Here, we review the current available information from all studies performed in TERC–/– mice providing information on the cardiovascular phenotypic characteristics. Although this mouse model has proven its value in the understanding of the role of telomere biology in cancer, stem cell, and basic telomere research, only few studies were specifically designed to answer cardiovascular-related questions. The TERC–/– mice provide exciting opportunities to expand our knowledge of telomere biology in cardiovascular disease and the potential identification of novel targets of treatment.

KEYWORDS Telomeres; Telomerase; Animal model; Cardiovascular phenotype

Time for primary review: 34 days


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