Telomere biology in heart failure

Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, Hanzeplein 1, 9700 RB Groningen, The Netherlands.
European Journal of Heart Failure (Impact Factor: 6.53). 10/2008; 10(11):1049-56. DOI: 10.1016/j.ejheart.2008.08.007
Source: PubMed


The incidence and prevalence of cardiovascular disease increases progressively with advancing age. Cardiovascular disease is a major cause of morbidity and mortality in Western Countries. In the near future, as the population ages, it is expected that the population prevalence of cardiovascular disease will increase dramatically, imposing a major social and economical burden on society. Not only is age closely related to the development and progression of cardiovascular disease, but genetic and environmental factors also play an important role. Recently, a chromosomal mechanism, telomere shortening, has been considered a driving force by which genetic and environmental factors jointly affect biological aging, and possibly the risk for developing age-associated diseases. Telomeres are the extreme ends of chromosomes and shorten progressively during every cell cycle and therefore can be considered an indicator of biological age. In heart failure, telomere length is severely reduced. In the current review, we will discuss the emerging role of telomere biology in the pathophysiology of heart failure.

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Available from: Rudolf Allert de Boer, Jan 09, 2015
    • "Telomeres and telomerase provide protection against threats to the genome that arise from aninherent difficulty in the asymmetric replication of DNA (Calado and Young, 2009). Recently, telomere and telomerase have been recognized as potential factors involved in the initiation and progression of cardiovascular disease (Samani and van der Harst, 2008; Fuster and Andres, 2006; Edo and Andres, 2005; Wong et al., 2008). There is accumulating evidence that connect telomere length with cardiovascular-related phenotypes, including atherosclerosis and heart failure (Wong et al., 2009). "
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    ABSTRACT: Abuse of anabolic androgenic steroids is linked to a variety of cardiovascular complications. The aim of our study was to investigate the possible cardiovascular effects of nandrolone decanoate on young rabbits using echocardiography, histology and monitoring of telomerase activity, oxidative stress and biochemical markers. Fourteen rabbits were divided into three administration groups and the control group. Doses of 4mg/kg and 10mg/kg of nandrolone decanoate, given intramuscularly and subcutaneously, two days per week for six months were applied. A 4-months wash-out period followed. Focal fibrosis and inflammatory infiltrations of cardiac tissue were observed in the high dose groups. Thiobarbituric Acid-Reactive Species (TBARS) levels were significantly increased in the high dose groups, while catalase activity decreased. Myocardial Performance Index (MPI) is the main echocardiographic index primarily affected by nandrolone administration in rabbits. Despite the preserved systolic performance, histological lesions observed associated with distorted MPI values, point to diastolic impairment of the thickened myocardium due to nandrolone treatment. Oxidative stress accumulates and telomerase activity in cardiac tissue rises. Subcutaneous administration seems to be more deleterious to the cardiovascular system, as oxidative stress, telomerase activity and biochemical markers do not appear to return into normal values in the wash-out period.
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    • "The exact cause of shorter telomeres in these individuals is not known. Some postulates are that high blood pressure, oxidative stress (caused by some other factor than excessive iron, such as smoking), tissue hypoperfusion, diabetes or atherosclerosis are also factors favouring the occurrence of heart failure and affecting telomere shortening (Wong et al., 2008). "
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    ABSTRACT: Oxidative stress can be induced by increased concentrations of iron in the body and consequently can cause shortening of telomeres. Telomeres, called mitotic clocks, are non-coding fragments at the end of chromosomes. During the replication of genetic material they are shortened, playing the role of ageing biomarkers in eukaryotes. In human endothelial cells, oxidative stress causes a decrease in telomerase activity. Shortening of chromosomes in telomeric parts was found in patients with primary hemochromatosis and in patients taking supplements containing iron. Increased level of transferrin saturation is associated with the presence of shorter telomeres in the chromosomes of leukocytes. The relationship between iron status and telomere length is still not fully understood.
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    • "Telomeres are specialized DNA structures made up of tandem repeats (TTAGGG in humans) located at the end of chromosomes [4, 5]. Telomeres have a critical function as they serve as protective caps, preventing the chromosomal ends to be accidently recognized as DNA double strands by the DNA damage–repair system, and activation of the p53 or p16INK4a pathway, which eventually leads to senescence or apoptosis. "
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    ABSTRACT: During normal aging, the heart undergoes functional, morphological and cellular changes. Although aging per se does not lead to the expression of heart failure, it is likely that age-associated changes lower the threshold for the manifestation of signs and symptoms of heart failure. In patients, the susceptibility, age of onset and pace of progression of heart failure are highly variable. The presence of conventional risk factors cannot completely explain this variability. Accumulation of DNA damage and telomere attrition results in an increase in cellular senescence and apoptosis, resulting in a decrease in the number and function of cells, contributing to the overall tissue and organ dysfunction. Biological aging, characterized by reduced telomere length, provides an explanation for the highly interindividual variable threshold to express the clinical syndrome of heart failure at some stage during life. In this review, we will elaborate on the current knowledge of aging of the heart, telomere biology and its potential role in the development of heart failure.
    Full-text · Article · Sep 2010 · Heart Failure Reviews
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