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A relationship exists between replicative senescence and cardiovascular health
A growing body of evidence demonstrates that the accumulation of senescent cells is a plausible ageing mechanism. It has been proposed that the senescence of vascular cells plays a causal role in the development of cardiovascular pathologies. A key prediction arising from this hypothesis is that cul...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3922945/ https://www.ncbi.nlm.nih.gov/pubmed/24472516 http://dx.doi.org/10.1186/2046-2395-2-3 |
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author | Karavassilis, Maria E Faragher, Richard |
author_facet | Karavassilis, Maria E Faragher, Richard |
author_sort | Karavassilis, Maria E |
collection | PubMed |
description | A growing body of evidence demonstrates that the accumulation of senescent cells is a plausible ageing mechanism. It has been proposed that the senescence of vascular cells plays a causal role in the development of cardiovascular pathologies. A key prediction arising from this hypothesis is that cultures of cells derived from donors with cardiovascular disease will show reduced in vitro replicative capacities compared to those derived from disease-free controls. Accordingly, we carried out a formal review of the relationship among donor age, cardiovascular health status and maximum population doubling level attained in vitro by cultures of vascular smooth muscle and endothelial cells. Data were available to us on a total of 202 independent cell cultures. An inverse relationship was found to exist between replicative capacity and donor age in both endothelial and vascular smooth muscle cells. Cultures derived from donors with cardiovascular disease showed a lower overall replicative potential than age-matched healthy controls. In general the replicative potential at the start of the lifespan was found to be higher in those individuals without disease than those with disease and the difference in average cumulative population doublings (CPDs) in age-matched individuals in the two groups remained roughly constant throughout the lifetime. These results are consistent with the model in which the inherited replicative capacity of vascular cells is a stronger determinant of the onset of cardiovascular disease later in life, than wear-and-tear throughout the life course. |
format | Online Article Text |
id | pubmed-3922945 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-39229452014-02-14 A relationship exists between replicative senescence and cardiovascular health Karavassilis, Maria E Faragher, Richard Longev Healthspan Review A growing body of evidence demonstrates that the accumulation of senescent cells is a plausible ageing mechanism. It has been proposed that the senescence of vascular cells plays a causal role in the development of cardiovascular pathologies. A key prediction arising from this hypothesis is that cultures of cells derived from donors with cardiovascular disease will show reduced in vitro replicative capacities compared to those derived from disease-free controls. Accordingly, we carried out a formal review of the relationship among donor age, cardiovascular health status and maximum population doubling level attained in vitro by cultures of vascular smooth muscle and endothelial cells. Data were available to us on a total of 202 independent cell cultures. An inverse relationship was found to exist between replicative capacity and donor age in both endothelial and vascular smooth muscle cells. Cultures derived from donors with cardiovascular disease showed a lower overall replicative potential than age-matched healthy controls. In general the replicative potential at the start of the lifespan was found to be higher in those individuals without disease than those with disease and the difference in average cumulative population doublings (CPDs) in age-matched individuals in the two groups remained roughly constant throughout the lifetime. These results are consistent with the model in which the inherited replicative capacity of vascular cells is a stronger determinant of the onset of cardiovascular disease later in life, than wear-and-tear throughout the life course. BioMed Central 2013-02-04 /pmc/articles/PMC3922945/ /pubmed/24472516 http://dx.doi.org/10.1186/2046-2395-2-3 Text en Copyright © 2013 Karavassilis and Faragher; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Karavassilis, Maria E Faragher, Richard A relationship exists between replicative senescence and cardiovascular health |
title | A relationship exists between replicative senescence and cardiovascular health |
title_full | A relationship exists between replicative senescence and cardiovascular health |
title_fullStr | A relationship exists between replicative senescence and cardiovascular health |
title_full_unstemmed | A relationship exists between replicative senescence and cardiovascular health |
title_short | A relationship exists between replicative senescence and cardiovascular health |
title_sort | relationship exists between replicative senescence and cardiovascular health |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3922945/ https://www.ncbi.nlm.nih.gov/pubmed/24472516 http://dx.doi.org/10.1186/2046-2395-2-3 |
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