Atherogenesis is the developmental process of atheromatous plaques.
2.
It is where small atheromatous plaques build up in the walls of medium and large arteries.
3.
Statins are the most frequently used lipid / cholesterol modifiers, which probably also stabilize existing atheromatous plaque.
4.
The muscular portion of artery walls usually remain strong, even after they have remodeled to compensate for the atheromatous plaques.
5.
M2 macrophages can remove cholesterol from blood vessels, but when the cholesterol is oxidized, the M2 macrophages become atheromatous plaque of atherosclerosis.
6.
The ensuing inflammation leads to formation of atheromatous plaques in the arterial tunica intima, a region of the vessel wall located between the endothelium and the tunica media.
7.
This was based on Constantinides s observation that circulating mast cell precursors could penetrate the open junctions between endothelial cells that line human atheromatous plaques in contrast to closed junctions over the normal arterial intima.
8.
The buildup of an atheromatous plaque is a slow process, developed over a period of several years through a complex series of cellular events occurring within the arterial wall and in response to a variety of local vascular circulating factors.
9.
While many of these products are used as markers of oxidative stress, the products derived from linoleic acid appear far more predominant than arachidonic acid products and therefore easier to identify and quantify in, for example, atheromatous plaques.
10.
Instead it was simply a remodeling of the atheromatous plaque, which was still protruding into the lumen of the artery after completion of angioplasty; the stenosis only appearing to be reduced because blood and contrast could now flow around and through some of the plaque.
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