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Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:807-808
doi: 10.1161/ATVBAHA.108.164434
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:807.)
© 2008 American Heart Association, Inc.


Editorials

Expanding the Concept of Telomere Dysfunction in Cardiovascular Disease

Pim van der Harst; Dirk J. van Veldhuisen; Nilesh J. Samani

From the Department of Cardiology (P.v.d.H., D.J.v.V), University Medical Center Groningen, University of Groningen, The Netherlands; and the Department of Cardiovascular Sciences (P.v.d.H., N.J.S.), University of Leicester, Glenfield Hospital, United Kingdom.

Correspondence to Dr P. van der Harst, Department of Cardiology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, 9700 RB Groningen, The Netherlands. E-mail p.van.der.harst@thorax. umcg.nl or pvdh1@le.ac.uk


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 


*    Introduction
 
Cellular repair and regeneration are considered important features of cardiovascular homeostasis. Exhaustion of these processes and replicative senescence during aging may promote cardiovascular diseases.1 This concept has recently received support from studies that used telomere length as a marker of biological aging and predictor of replicative senescence.1 Further studies show that shorter telomere length, which indicates older cells, is associated with several types of cardiovascular diseases including atherosclerosis2 and heart failure3 (Figure). Most of the studies to date have used white blood cell telomere length as a marker of ageing, but these might not necessarily be the most relevant cells to study.


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Figure. A, Telomeres (red) are located on the extreme ends of the chromosome (green). B, Hypothetical effects on BM stem cells, lymphocytes, and granulocytes of known factors determining telomere length, include replicative stress, risk factors (eg, oxidative stress), and the strong genetic determinant. C, The potential levels on which the association between telomere length and the cardiovascular disease continuum (D) may lie. BM indicates bone marrow; WBC, white blood cells, CAD, coronary artery disease; CHF, chronic heart failure.

See accompanying article on page 968


*    Current Study
 
There is evidence that cells originating from the bone marrow contribute to cardiovascular repair and outcome.4,5 In the current issue of Arteriosclerosis, Thrombosis, and Vascular Biology,6 Spyridopoulos et al focus on these cells and expand the evidence for the association between telomere biology and cardiovascular disease. They report a number of novel observations. First, they report a correlation between bone marrow . . . [Full Text of this Article]


Related Article:

Telomere Gap Between Granulocytes and Lymphocytes Is a Determinant for Hematopoetic Progenitor Cell Impairment in Patients With Previous Myocardial Infarction
Ioakim Spyridopoulos, Young Erben, Tim H. Brummendorf, Judith Haendeler, Klaus Dietz, Florian Seeger, Christine K. Kissel, Hans Martin, Jedrzej Hoffmann, Birgit Assmus, Andreas M. Zeiher, and Stefanie Dimmeler
Arterioscler Thromb Vasc Biol 2008 28: 968-974. [Abstract] [Full Text] [PDF]



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