Le vieillissement de la paroi artérielle

Abstract

Several changes in structure and function of the arterial wall have been described in association with aging. In the media, elastic fibers show fragmentations, and the collagen/elastin ratio is increased. Glycated proteins that accumulate in aging make collagen fibers more rigid and resistant to proteolysis. Aged smooth muscle cells dedifferentiate into a proliferative and synthetic phenotype, probably responsible for medial and intimal fibrosis. The morphological aspects of the endothelium are not substantially modified in aging, even though some endothelial functions are altered, in particular endothelium-dependent relaxation, prostacyclin release, as well as the endothelial barrier function. The sub-endothelial space is strikingly thickened in aging. This layer contains collagen fibers, proteoglycans, as well as smooth muscle cells, and mononuclear cells normally absent in young arteries. Precise mechanisms and chronology of the aging process in the arterial wall are not well understood, and the main explicative hypotheses are reviewed. Moreover, interactions between aging and arterial diseases - hypertension and atherosclerosis - are discussed.