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Telomere Biology and Vascular Aging

Frej, Fyhrquist and Peter, M. Nilsson LU (2015) p.201-211
Abstract

Telomeres form the end segment of the DNA helix and shorten with every cell division until getting so short that the cell stops dividing and will undergo programmed cell death (apoptosis). Research has supported the view that telomere length could be regarded as a marker of biological aging, even if methodological problems could interfere with the interpretation of telomere length in cross-sectional studies when causality cannot be proven. Ideally the telomere attrition rate should be calculated based on repeated measurements during follow-up. So far, epidemiological studies have supported the role of short telomeres being predictive of coronary heart disease (CHD) events but not stroke, based on meta-analysis. A genetic risk score... (More)

Telomeres form the end segment of the DNA helix and shorten with every cell division until getting so short that the cell stops dividing and will undergo programmed cell death (apoptosis). Research has supported the view that telomere length could be regarded as a marker of biological aging, even if methodological problems could interfere with the interpretation of telomere length in cross-sectional studies when causality cannot be proven. Ideally the telomere attrition rate should be calculated based on repeated measurements during follow-up. So far, epidemiological studies have supported the role of short telomeres being predictive of coronary heart disease (CHD) events but not stroke, based on meta-analysis. A genetic risk score based on several genetic markers of telomere biology is associated with CHD risk, which proves that a true causal and unconfounded relationship may exist. Future intervention studies will hopefully reveal whether telomere length is possible to influence by lifestyle improvements or drug therapy in randomized, controlled studies.

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Please use this url to cite or link to this publication:
author
organization
publishing date
type
Chapter in Book/Report/Conference proceeding
publication status
published
subject
keywords
Cardiovascular, Cell, DNA, Leukocyte, Quantitative PCR, Southern blot, Telomere, Vascular aging
host publication
Early Vascular Aging (EVA)
editor
Nilsson, Peter M.; Olsen, Michael H.; Laurent, St├ęphane; ; and
pages
11 pages
publisher
Oxford: Elsevier Science Ltd
external identifiers
  • scopus:85072344109
ISBN
9780128016763
9780128013878
DOI
10.1016/B978-0-12-801387-8.00020-X
language
English
LU publication?
yes
id
af0c9b4c-bb5b-4af4-84ae-8852cd5d37dd
date added to LUP
2019-10-01 08:43:36
date last changed
2019-10-23 06:23:29
@inbook{af0c9b4c-bb5b-4af4-84ae-8852cd5d37dd,
  abstract     = {<p>Telomeres form the end segment of the DNA helix and shorten with every cell division until getting so short that the cell stops dividing and will undergo programmed cell death (apoptosis). Research has supported the view that telomere length could be regarded as a marker of biological aging, even if methodological problems could interfere with the interpretation of telomere length in cross-sectional studies when causality cannot be proven. Ideally the telomere attrition rate should be calculated based on repeated measurements during follow-up. So far, epidemiological studies have supported the role of short telomeres being predictive of coronary heart disease (CHD) events but not stroke, based on meta-analysis. A genetic risk score based on several genetic markers of telomere biology is associated with CHD risk, which proves that a true causal and unconfounded relationship may exist. Future intervention studies will hopefully reveal whether telomere length is possible to influence by lifestyle improvements or drug therapy in randomized, controlled studies.</p>},
  author       = {Frej, Fyhrquist and Peter, M. Nilsson},
  editor       = {Nilsson, Peter M. and Olsen, Michael H. and Laurent, St├ęphane},
  isbn         = {9780128016763},
  keyword      = {Cardiovascular,Cell,DNA,Leukocyte,Quantitative PCR,Southern blot,Telomere,Vascular aging},
  language     = {eng},
  month        = {01},
  pages        = {201--211},
  publisher    = {Oxford: Elsevier Science Ltd},
  title        = {Telomere Biology and Vascular Aging},
  url          = {http://dx.doi.org/10.1016/B978-0-12-801387-8.00020-X},
  year         = {2015},
}