Thursday, 13 October 2016

Intracellular Zinc: A mediator of Vascular Aging and Disease?

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.

Intracellular ZincVascular Aging 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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