Abstract
Vascular cells in normal adult mammals, including humans, appear to be relatively quiescent populations with respect to growth. In particular, mitotic figures are rarely seen in the endothelial lining of large and small blood vessels, and the low levels of DNA synthesis detectable by tritiated thymidine autoradiography usually have been attributed to a process of cell replacement. Similarly, the smooth muscle cells that comprise the medial layer of the aorta and its major branches normally show little evidence of turn-over. However, this slow renewal pattern can be increased dramatically, in both vascular endothelium and smooth muscle, by a variety of physiologic and pathologic stimuli. Thus, endothelial proliferation is a prominent feature in such processes as wound healing, the organization of myocardial infarcts and intravascular clots, and the growth of solid tumors (1). In addition, hyperplasia of arterial smooth muscle, in response to intimai injury, is thought to be an early event in the development of atherosclerotic lesions (2, 3).
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Gimbrone, M.A. (1984). Macrophages, neovascularization, and the growth of vascular cells. In: Jaffe, E.A. (eds) Biology of Endothelial Cells. Developments in Cardiovascular Medicine, vol 27. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2825-4_10
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DOI: https://doi.org/10.1007/978-1-4613-2825-4_10
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