Telomere shortening, atherosclerosis, and metabolic syndrome.

This mechanism resembles inflammatory reactions to exogenous factors and the wound healing process (2). Dysfunction of vascular endothelial cells is thought to induce a cascade of pathologic reactions of cell groups mediated by the expression of adhesion molecules, resulting in infiltration of mononuclear cells, foam cell formation, promotion of thrombus formation, and disturbed relaxation of blood vessels. Eukaryotic chromosomes end with telomeres, which comprise tandem repeats of the sequence TTAGGG, and are involved in the stabilization of chromosomal ends. It is well known that telomeres progressively shorten with repeated cell division and aging. There is a negative correlation between age and telomere length of peripheral blood mononuclear cells. It has been suggested that the cellular dysfunction that accompanies senescence of vascular cells could contribute to the development of atherosclerosis. Recent studies have demonstrated that telomere shortening is related to various pathological conditions including atherosclerosis (3).