Aging of the vascular-wall and atherosclerosis.
The rapid increase of life expectancy during the last half of the 20th century is changing the expression of cardiovascular disease and of its risk factors. These findings are examined by the separate consideration of atheromatous plaque formation and vascular wall stiffening, known as arteriosclerosis. in humans, these processes may progress together, but in some other species as the rat, only vascular wall stiffening is observed. A saturated fat- and cholesterol-rich diet produces the early appearance of lipidic plaques, which progress to fibrous, sometimes ulcerated, thrombotic lesions. This progression is age dependent; the establishment of lipidic plaques is not. Vascular wall stiffening, characterized by an increase of the collagen-elastin ratio and diffuse deposition of calcium and lipids is also age dependent (arteriosclerosis). Although hyperlipidemia appears to be involved both in plaque formation and wall thickness progression, the detailed mechanisms are not identical. In the oldest age group (above 80 years and in centenarians), high cholesterol values may not be a risk factor as in younger individuals. Among the cellular and molecular mechanisms involved, immune factors and modifications in receptor coupling appear to play a major role. These mechanisms are described in some detail.
Robert
L
L
Centre de Recherche Bioclinique sur le Vieillissement, Groupe Hospitalier Charles Foix-Jean Rostand, 94205, Ivry sur Seine, France. 106517.545@compuserve.com
D000375:Aging / Q000473:pathology*; D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology* / Q000276:immunology; D001808:Blood Vessels / Q000473:pathology*; D002318:Cardiovascular Diseases / Q000209:etiology; D006801:Humans; D011956:Receptors, Cell Surface / Q000502:physiology; D017474:Receptors, Laminin / Q000502:physiology
D011956:Receptors, Cell Surface; D017474:Receptors, Laminin; C054901:elastin-binding proteins