Cellular aging in cardiovascular diseases

As we progress to a society with an increasing average age, the problems that are associated with advanced age becoming more prominent. This is particularly visible by the increase onset of aging associated diseases, such as atherosclerosis, heart failure and diabetes mellitus type II. On a cellular level, the process of cellular aging is termed cellular senescence and the number of senescent cells in an organism increases in an age dependent manner. In our research we focused on the presence and development of cellular senescence in cardiovascular diseases. The role of the telomeres and the enzyme telomerase during aging, and in cardiovascular diseases is discussed. In a model for telomere shortening we describe that telomere length is associated with a striking decrease in voluntary exercise, but this was not directly associated with a cardiovascular phenotype.
In the second part of this thesis we focus more on endothelial senescence and the pathways that are involved in the prevention of senescence. In endothelial cell culture models and in a model for diabetes type II we show that cellular senescence can be prevented by activating specific receptors that are present on the endothelial cells. Although these results have to be extended with studies in a human population, these results give new fundamental insights into the development of cellular senescence and open up new targets that eventually might help to fight the deleterious effects of cellular aging in cardiovascular diseases.

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