Copyright © 2004, European Society of Cardiology
Aging, telomeres, and atherosclerosis
Laboratory of Vascular Biology, Department of Molecular and Cellular Pathology and Therapy, Instituto de Biomedicina de Valencia, C/Jaime Roig 11, 46010, Valencia, Spain
* Corresponding author. Tel.: +34 96 3391752; fax: +34 96 3391751. Email address: vandres{at}ibv.csic.es
Although the level and pace of population aging display high geographical variability, virtually all countries have been experiencing growth in their elderly population, particularly in developed nations. Because aging is a major risk factor for atherosclerosis and associated disease, it is of up most importance to unravel the molecular mechanisms involved in vascular aging. Telomeres are specialized DNA-protein structures located at the ends of eukaryotic chromosomes whose length is progressively reduced in most somatic cells during aging. It is accepted that telomere exhaustion contributes to organismal ageing at least by impairing cell proliferation and viability. An emerging question is whether telomere erosion contributes to atherosclerosis. Here we discuss recent advances on the molecular control of telomere length in vascular cells, as well as animal and human studies that address the role of telomeres in vascular pathobiology. Although the interrelationships between telomere length and cardiovascular disease appear obvious, a chief question that remains unanswered is whether telomere ablation is cause of vascular injury or a surrogate phenomenon.
KEYWORDS Aging; Telomeres; Telomerase; Atherosclerosis; Hypertension; Diabetes
Time for primary review 23 days
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  K. Kublickiene, X.-D. Fu, E. Svedas, B.-M. Landgren, A. R. Genazzani, and T. Simoncini Effects in Postmenopausal Women of Estradiol and Medroxyprogesterone Alone and Combined on Resistance Artery Function and Endothelial Morphology and Movement J. Clin. Endocrinol. Metab., May 1, 2008; 93(5): 1874 - 1883. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Q. Shi, G. B. Hubbard, R. S. Kushwaha, D. Rainwater, C. A. Thomas III, M. M. Leland, J. L. VandeBerg, and X. L. Wang Endothelial senescence after high-cholesterol, high-fat diet challenge in baboons Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H2913 - H2920. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Nitenberg Macrovascular disease in type 2 diabetes: We do need animal models for in vivo studies Cardiovasc Res, February 1, 2007; 73(3): 450 - 452. [Full Text] [PDF]
|
|
|
|
|
|
H. M. Piper and E. A. Martinson Cardiovascular Research speeds up-Even more Cardiovasc Res, March 1, 2006; 69(4): 773 - 776. [Full Text] [PDF]
|
|
|
|
|
|
S. Pepe and E. G. Lakatta Aging hearts and vessels: Masters of adaptation and survival Cardiovasc Res, May 1, 2005; 66(2): 190 - 193. [Full Text] [PDF]
|
|