Aging is a major risk factor in the development
of cardiovascular diseases. Accumulation of waste materials like damaged
mitochondria and decline in stress response mechanisms contribute to increased
oxidative stress over time. The free radical theory of aging postulates that
increased levels of reactive oxygen species [ROS] cause genomic and
mitochondrial DNA damage leading to sustained oxidative stress that promotes
tissue dysfunction and aging. In the cardiovascular system, NADPH oxidasesproduce ROS that are involved in normal function; however, overproduction ofROS by these enzymes, as well as decreased expression of antioxidant enzymes
are associated with vascular dysfunction and disease.
Cellular senescence, a hallmark of mammalian
aging, is a process of permanent cell cycle arrest that has been linked to the development of
age-related diseases, including atherosclerosis. A causative role for
senescence in disease development was reported as the selective removal of
senescent cells in vivo showed a delay in age-related diseases. Although
senescent cells have lost their replicative capability, they possess a
secretory and pro-oxidative/inflammatory phenotype that likely contributes to organ dysfunction
during aging.
It
is well known that nutritional status plays an important role in disease
development. Over-consumption of high calorie foods is a risk factor for
diseases like metabolic syndrome, atherosclerosis and diabetes; however less is
known about the consequences of micronutrient deficiencies in cardiovascular
disease progression. Read more............
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