Abstract
The aging process is associated with a loss of complexity in the dynamics of physiological systems that reduce the ability to adapt to stress, causing frailty and/or age-related diseases. At the cellular level, proliferative and/or oxidative-stress induced cell senescence associated with a pro-inflammatory state may greatly contribute to age-associated impaired tissue and organ functions. Senescence of endothelial and cardiac cells observed over normal aging, appear to be accelerated in age-related diseases and in particular, in cardiovascular disease (CVD). Although the molecular mechanisms of cellular senescence have been extensively studied, a complete understanding of their role in CVD is still limited. Cardiac, endothelial (EC), vascular smooth muscle (VSMC), leukocytic and stem cells (endothelial progenitor cells (EPC), embryonic stem cells (ESC) and haematopoietic stem cells (HSC)) may play a pivotal role on the maintenance and regeneration of cardiovascular tissue. Age-associated changes of such cells may enhance the risk of developing CVD. The purpose of this review is to illustrate how cellular senescence may affect tissue repair and maintenance toward CVD, focusing on the role played by telomere length and microRNA expression. Finally, interventions aimed at improving the age-related decline in vascular cells during aging and disease, as well as strategies to harness the regenerative capacity of stem cells in CVD will be discussed.
| Original language | English |
|---|---|
| Pages (from-to) | 1710-1719 |
| Number of pages | 10 |
| Journal | Current Pharmaceutical Design |
| Volume | 19 |
| Issue number | 9 |
| Publication status | Published - 2013 |
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Keywords
- Cellular senescence
- microRNA
- Progenitor endothelial cells
- Telomere length
ASJC Scopus subject areas
- Drug Discovery
- Pharmacology
Cite this
Cellular senescence in cardiovascular diseases : Potential age-related mechanisms and implications for treatment. / Olivieri, Fabiola; Recchioni, Rina; Marcheselli, Fiorella; Abbatecola, Angela Marie; Santini, Gabriele; Borghetti, Giulia; Antonicelli, Roberto; Procopio, Antonio Domenico.
In: Current Pharmaceutical Design, Vol. 19, No. 9, 2013, p. 1710-1719.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Cellular senescence in cardiovascular diseases
T2 - Potential age-related mechanisms and implications for treatment
AU - Olivieri, Fabiola
AU - Recchioni, Rina
AU - Marcheselli, Fiorella
AU - Abbatecola, Angela Marie
AU - Santini, Gabriele
AU - Borghetti, Giulia
AU - Antonicelli, Roberto
AU - Procopio, Antonio Domenico
PY - 2013
Y1 - 2013
N2 - The aging process is associated with a loss of complexity in the dynamics of physiological systems that reduce the ability to adapt to stress, causing frailty and/or age-related diseases. At the cellular level, proliferative and/or oxidative-stress induced cell senescence associated with a pro-inflammatory state may greatly contribute to age-associated impaired tissue and organ functions. Senescence of endothelial and cardiac cells observed over normal aging, appear to be accelerated in age-related diseases and in particular, in cardiovascular disease (CVD). Although the molecular mechanisms of cellular senescence have been extensively studied, a complete understanding of their role in CVD is still limited. Cardiac, endothelial (EC), vascular smooth muscle (VSMC), leukocytic and stem cells (endothelial progenitor cells (EPC), embryonic stem cells (ESC) and haematopoietic stem cells (HSC)) may play a pivotal role on the maintenance and regeneration of cardiovascular tissue. Age-associated changes of such cells may enhance the risk of developing CVD. The purpose of this review is to illustrate how cellular senescence may affect tissue repair and maintenance toward CVD, focusing on the role played by telomere length and microRNA expression. Finally, interventions aimed at improving the age-related decline in vascular cells during aging and disease, as well as strategies to harness the regenerative capacity of stem cells in CVD will be discussed.
AB - The aging process is associated with a loss of complexity in the dynamics of physiological systems that reduce the ability to adapt to stress, causing frailty and/or age-related diseases. At the cellular level, proliferative and/or oxidative-stress induced cell senescence associated with a pro-inflammatory state may greatly contribute to age-associated impaired tissue and organ functions. Senescence of endothelial and cardiac cells observed over normal aging, appear to be accelerated in age-related diseases and in particular, in cardiovascular disease (CVD). Although the molecular mechanisms of cellular senescence have been extensively studied, a complete understanding of their role in CVD is still limited. Cardiac, endothelial (EC), vascular smooth muscle (VSMC), leukocytic and stem cells (endothelial progenitor cells (EPC), embryonic stem cells (ESC) and haematopoietic stem cells (HSC)) may play a pivotal role on the maintenance and regeneration of cardiovascular tissue. Age-associated changes of such cells may enhance the risk of developing CVD. The purpose of this review is to illustrate how cellular senescence may affect tissue repair and maintenance toward CVD, focusing on the role played by telomere length and microRNA expression. Finally, interventions aimed at improving the age-related decline in vascular cells during aging and disease, as well as strategies to harness the regenerative capacity of stem cells in CVD will be discussed.
KW - Cellular senescence
KW - microRNA
KW - Progenitor endothelial cells
KW - Telomere length
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UR - http://www.scopus.com/inward/citedby.url?scp=84876707441&partnerID=8YFLogxK
M3 - Article
C2 - 23061728
AN - SCOPUS:84876707441
VL - 19
SP - 1710
EP - 1719
JO - Current Pharmaceutical Design
JF - Current Pharmaceutical Design
SN - 1381-6128
IS - 9
ER -