Abstract
Atherosclerosis is now recognised as a multifactorial disease process in which a number of distinct but overlapping pathways of pathogenesis are involved. The major current hypotheses of atherogenesis focus on (a) response of the arterial wall to injury, (b) lipid infiltration into the intima, (c) smooth muscle cell transformation, (d) thrombosis, (e) immune mechanisms and (f) viruses as aetiological agents (Ross 1986; Steinberg et al. 1989; Scott 1989; Penn et al. 1986; Libby and Hansson 1991; Hajjar 1991). These hypotheses are not mutually exclusive, but reflect different aspects of an interactive disease process in which various factors may assume different degrees of importance in different stages and instances of the disease. Underlying all these processes is a complex web of interactions between the cellular constituents of the arterial wall, their secreted products and lipoproteins.
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Robenek, H., Severs, N.J. (1993). Lipoprotein Receptors on Macrophages and Smooth Muscle Cells. In: Roessner, A., Vollmer, E. (eds) Recent Progress in Atherosclerosis Research. Current Topics in Pathology, vol 87. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76849-1_4
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