Abstract
Much progress has been made in last two decades in research, prevention, and treatment of atherosclerosis and subsequent coronary heart diseases. Hypotheses have been proposed to define a unifying concept for the basic mechanisms of atherogenesis. The response-to-injury hypothesis, as recently updated (Ross, 1993a,b), suggests that various forms of insults to the endothelium and arterial cells initiate a chronic, inflammatory response featuring the subendothelial infiltration and activation of macrophages and T-cells. Upregulation of expression and secretion of cytokines and growth factors associated with these activated leukocytes result in smooth muscle cell (SMC) migration and proliferation into the intima of the arterial wall. Simultaneous with this process is thought to be the modification of lipoproteins in the arterial wall. In one such process low-density lipoproteins (LDL) can be oxidatively modified and taken up by macrophages to become foam cells (Steinberg et al., 1989). Because it is cytotoxic, oxidized LDL may kill macrophages and endothelial cells. In response to endothelial injury, platelets adhere, aggregate and secrete platelet-derived growth factor (PDGF), which further stimulates the proliferation of SMCs and thrombosis as proposed in the original response-to-injury hypothesis (Ross and Glomset, 1976).
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Shih, J.C.H., Kelemen, D.W. (1995). Possible Role of Viruses in Atherosclerosis. In: Longenecker, J.B., Kritchevsky, D., Drezner, M.K. (eds) Nutrition and Biotechnology in Heart Disease and Cancer. Advances in Experimental Medicine and Biology, vol 369. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1957-7_9
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