Endothelin, Cell Proliferation and Atherosclerosis
Tissue injury, macrophage infiltration, abnormal proliferation and migration of vascular smooth muscle cells, hypercholesterolaemia and the resultant accumulation of excess lipids, together with excess calcium deposition, are all intimately involved in the atherosclerotic process. The trigger for the development of the lesion is probably best accounted for in terms of the “response to injury” hypothesis originally proposed by Ross (Ross 1986). According to this hypothesis a variety of “injury promoted” growth factors — including platelet derived growth factor (PDGF), epidermal growth factor (EGF) and transforming growth factor β (TGFβ) stimulate both the migration of medial vascular smooth muscle cells into the arterial intima and their subsequent replication (Ross 1986; Schwartz et al. 1986). The lipid- loading of these cells and the subsequent formation of the fibrous “cap” are really only the terminal events (Figure 15.1).
KeywordsVascular Smooth Muscle Cell Calcium Antagonist Smooth Muscle Cell Proliferation Vascular Smooth Muscle Cell Proliferation Thymidine Uptake
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