Abstract
Elastin fibres give blood vessels important rheological properties, such as the postsystolic elastic recoil. The age-dependent increase of Ca2+ and lipid content, and elastolytic degradation of the fibres progressively impairs their function and produces circulating elastin peptides. Their interaction with the elastin receptor on smooth muscle cells induces not only increased cell-elastin fibre adhesion and endothelium-dependent vasorelaxation but also the release of lytic enzymes and oxygen free radicals from monocytes penetrating the vascular wall during atherogenesis. The age-dependent 'uncoupling' of the receptor has been shown to be involved in the loss of Ca2+ homeostatic mechanisms and the progressive calcification of the vessel wall.
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