Aging, telomeres, and atherosclerosis.     

 Edo, Maria Dolores; Andres, Vicente.    Laboratory of Vascular Biology, Department of Molecular and Cellular Pathology and Therapy,  Instituto de Biomedicina de Valencia,  Valencia,  Spain.    Cardiovascular Research  (2005),  66(2),  213-221.  Publisher: Elsevier B.V.,  CODEN: CVREAU  ISSN: 0008-6363.  Journal; General Review  written in English.    CAN 142:427532    AN 2005:326162    CAPLUS   (Copyright (C) 2008 ACS on SciFinder (R))  

Abstract

A review.  Although the level and pace of population aging display high geog. 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 assocd. disease, it is of up most importance to unravel the mol. 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.  The authors discuss recent advances on the mol. control of telomere length in vascular cells, as well as animal and human studies that address the role of telomeres in vascular pathobiol.  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.