[Aging of arterial extracellular matrix elastin: etiology and consequences]

This review discusses the hypothesis that the accumulation with advancing age of physical insults to the arterial wall (pressure, flow, diameter) may induce fragmentation of the medial elastic network, thereby leading to cardiovascular dysfunction. Physical factors have been shown to alter medial cell activity, inducing medial hypertrophy and other changes. Their potential contribution to changes in extracellular matrix proteins (perhaps mediated by integrins) has been less extensively studied. A metabolic factor may also be involved in age-related elastic fiber fragmentation. Oxidative stress in the arterial wall increases with age and leads to an increase in the production of cytokines, which stimulate the activity of elastases. Changes in elastic fiber composition may be associated with a greater propensity for calcification. Elastic fiber architecture can be modified by three reactions, namely elastolysis, elastocalcinosis, and production of new elastin fibers. These changes in the elastic network may have a number of consequences. Dilatation may shift strain to collagen, resulting in increases in the elastic modulus and impedance of the arterial wall. In turn, these changes may modify ventricle-artery coupling, leading to left ventricular hypertrophy (an independent risk factor for cardiovascular morbidity and mortality in elderly individuals). The increase in arterial wall elastic modulus associated with arteriosclerosis, together with arterial dilatation and flow profile changes, may also increase the susceptibility of the arterial wall to atheroma lesions.