Platelets, platelet-derived growth factor, growth control, and their interactions with the vascular wall.
The response-to-injury hypothesis of atherosclerosis describes how risk factors associated with atherogenesis may alter endothelial function, creating opportunities for endothelial cell separation and interactions with blood monocyte/macrophages and platelets that result in the intimal proliferative smooth-muscle lesions of atherosclerosis. Growth factors derived from platelets (platelet-derived growth factor) and macrophages (macrophage-derived growth factor) are described and their possible role in atherogenesis is presented. Possible approaches for the prevention of atherosclerosis include the development of means of interfering with the activity of these growth factors.
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D000818:Animals; D001161:Arteriosclerosis / Q000188:drug therapy / Q000209:etiology* / Q000517:prevention & control; D001792:Blood Platelets / Q000502:physiology*; D001808:Blood Vessels / Q000502:physiology*; D006801:Humans; D008264:Macrophages / Q000502:physiology; D010982:Platelet-Derived Growth Factor / Q000502:physiology*; D011956:Receptors, Cell Surface / Q000032:analysis; D017479:Receptors, Platelet-Derived Growth Factor
D010982:Platelet-Derived Growth Factor; D011956:Receptors, Cell Surface; D017479:Receptors, Platelet-Derived Growth Factor