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Telomeres and atherosclerosis.

Khan S, Chuturgoon AA, Naidoo DP - Cardiovasc J Afr (2012)

Bottom Line: Studies have consistently demonstrated an association between shortened telomere length and coronary artery disease (CAD).Several of the CAD risk factors and particularly type 2 diabetes are linked to telomere shortening and cellular senescence.We review the evidence linking telomere biology to atherosclerosis and discuss methods to preserve telomere length.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Cardiology, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, Durban, South Africa. khans19@ukzn.ac.za

ABSTRACT
In humans and other multicellular organisms that have an extended lifespan, the leading causes of death are atherosclerotic cardiovascular disease and cancer. Experimental and clinical evidence indicates that these age-related disorders are linked through dysregulation of telomere homeostasis. Telomeres are DNA protein structures located at the terminal end of chromosomes and shorten with each cycle of cell replication, thereby reflecting the biological age of an organism. Critically shortened telomeres provoke cellular senescence and apoptosis, impairing the function and viability of a cell. The endothelial cells within atherosclerotic plaques have been shown to display features of cellular senescence. Studies have consistently demonstrated an association between shortened telomere length and coronary artery disease (CAD). Several of the CAD risk factors and particularly type 2 diabetes are linked to telomere shortening and cellular senescence. Our interest in telomere biology was prompted by the high incidence of premature CAD and diabetes in a subset of our population, and the hypothesis that these conditions are premature-ageing syndromes. The assessment of telomere length may serve as a better predictor of cardiovascular risk and mortality than currently available risk markers, and anti-senescence therapy targeting the telomere complex is emerging as a new strategy in the treatment of atherosclerosis. We review the evidence linking telomere biology to atherosclerosis and discuss methods to preserve telomere length.

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Related in: MedlinePlus

A simplified scheme depicting the structure of the telomere and its location on the chromosome in the cell. Reproduced with permission.126
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Figure 1: A simplified scheme depicting the structure of the telomere and its location on the chromosome in the cell. Reproduced with permission.126

Mentions: Telomeres have a dynamic structure that is thought to switch between a closed, protected state and an open, extendable state, which allows the DNA terminus to undergo replication. The protected state is necessary for safeguarding the integrity of genomic material, whereas the extendable state allows the enzyme telomerase to extend short telomeres (Figs 1, 2).31 Telomere components include:


Telomeres and atherosclerosis.

Khan S, Chuturgoon AA, Naidoo DP - Cardiovasc J Afr (2012)

A simplified scheme depicting the structure of the telomere and its location on the chromosome in the cell. Reproduced with permission.126
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3721896&req=5

Figure 1: A simplified scheme depicting the structure of the telomere and its location on the chromosome in the cell. Reproduced with permission.126
Mentions: Telomeres have a dynamic structure that is thought to switch between a closed, protected state and an open, extendable state, which allows the DNA terminus to undergo replication. The protected state is necessary for safeguarding the integrity of genomic material, whereas the extendable state allows the enzyme telomerase to extend short telomeres (Figs 1, 2).31 Telomere components include:

Bottom Line: Studies have consistently demonstrated an association between shortened telomere length and coronary artery disease (CAD).Several of the CAD risk factors and particularly type 2 diabetes are linked to telomere shortening and cellular senescence.We review the evidence linking telomere biology to atherosclerosis and discuss methods to preserve telomere length.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Cardiology, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, Durban, South Africa. khans19@ukzn.ac.za

ABSTRACT
In humans and other multicellular organisms that have an extended lifespan, the leading causes of death are atherosclerotic cardiovascular disease and cancer. Experimental and clinical evidence indicates that these age-related disorders are linked through dysregulation of telomere homeostasis. Telomeres are DNA protein structures located at the terminal end of chromosomes and shorten with each cycle of cell replication, thereby reflecting the biological age of an organism. Critically shortened telomeres provoke cellular senescence and apoptosis, impairing the function and viability of a cell. The endothelial cells within atherosclerotic plaques have been shown to display features of cellular senescence. Studies have consistently demonstrated an association between shortened telomere length and coronary artery disease (CAD). Several of the CAD risk factors and particularly type 2 diabetes are linked to telomere shortening and cellular senescence. Our interest in telomere biology was prompted by the high incidence of premature CAD and diabetes in a subset of our population, and the hypothesis that these conditions are premature-ageing syndromes. The assessment of telomere length may serve as a better predictor of cardiovascular risk and mortality than currently available risk markers, and anti-senescence therapy targeting the telomere complex is emerging as a new strategy in the treatment of atherosclerosis. We review the evidence linking telomere biology to atherosclerosis and discuss methods to preserve telomere length.

Show MeSH
Related in: MedlinePlus