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Open Access Highly Accessed Review

A relationship exists between replicative senescence and cardiovascular health

Maria E Karavassilis1 and Richard Faragher2*

Author Affiliations

1 School of Medicine, The Commonwealth Building, The Hammersmith Hospital, Imperial College London, Du Cane Road, W12 0NN, London, UK

2 School of Pharmacy and Biomolecular Sciences, University of Brighton, Huxley Building, Lewes Road, BN2 4GJ, Brighton, UK

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Longevity & Healthspan 2013, 2:3  doi:10.1186/2046-2395-2-3

Published: 4 February 2013

Abstract

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.

Keywords:
Replicative senescence; Vascular endothelial cells; Vascular smooth muscle cells; Ageing; Atherosclerosis; Hypertension