Abstract

Telomeres, or historically named "terminal genes" are first discovered by Muller working on fruit fly in 1930s. Since then, the great progress was made in understanding the consequences of telomere erosion on the human health and disease states, as age related vascular diseases. The overlapping links between telomere dynamics in endothelial cells, endothelial progenitor cells and other cells laid in the vessel wall made telomere regulation as a hub node in keeping vascular health. Shortest telomeres paralleled with the advent of coronary artery diseases and its related risk factors, is well explainable by "Telomere hypothesis". But this needs further studies to determine the real state of short telomere length in atherosclerosis: marker or risk factor? As a marker, leukocyte telomere length was used in mirroring mean telomere length of the whole organism, but there are some debates about the best cell reflecting the exact telomere length. Impact of telomere biology on vascular system in the progression and development of atherosclerosis delights its targeting as a new therapeutic option for cardiovascular diseases. This needs in depth elucidation of the underlying mechanisms of telomere erosion in vascular beds.

Key words: Telomere length, endothelial cell dysfunction, atherosclerosis.

Abbreviation

ATM, Ataxia telangiectasia mutated; ADP, adenosine diphosphate;PARPS, poly(ADP-ribosyl)polymerases; vWF, von Willebrand factor; TERT,Telomerase Reverse Transcriptase; TEP, telomerase associated protein; EPCS,endothelial progenitor cells; EVA, early vascular aging; TMM, telomere maintenance mechanisms; SSDB, single-stranded DNA breaks; eNOS, endothelial nitric oxide synthase; RNP, ribonucleoprotein; HR, homologues recombination;NHEJR, non-homologues end joining replication; ALT, alternative lengthening of telomere; LTL, Leukocyte telomere length; STELA, single telomere length analysis.