Title:Cellular Senescence in Cardiovascular Diseases: Potential Age-Related Mechanisms and Implications for Treatment
Volume: 19
Issue: 9
Author(s): Fabiola Olivieri, Rina Recchioni, Fiorella Marcheselli, Angela Marie Abbatecola, Gabriele Santini, Giulia Borghetti, Roberto Antonicelli and Antonio Domenico Procopio
Affiliation:
Keywords:
Cellular senescence, telomere length, microRNA, progenitor endothelial cells, aging, stress, cardiovascular disease (CVD), embryonic stem cells (ESC), haematopoietic stem cells (HSC), vascular cells
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.
