In their analysis of the genesis of atherosclerosis, Ross and Glomset1 postulate that accumulations of smooth muscle cells in the arterial tunica intima between the endothelium and the fenestrated internal elastic lamina represent the start of lesions. Early in life, such cells are scarce, but their number increases with aging, thereby thickening the intima. The authors contend that the intimal increase in smooth muscle cells, accompanied by deposition of intracellular and extracellular lipid and connective tissue, is in fact the disease, atherosclerosis.
Whether the increased numbers of smooth muscle cells derive from preexisting cells or originate by migration of smooth muscle cells through the internal elastic lamina has not been clarified. In any event, the accumulations occur mainly at arterial branch points where endothelial structure is thought to be under greater hemodynamic stress, and intimal accumulation of smooth muscle cells can be produced experimentally by injuring the endothelium.
In vivo