Atherogenesis is a multi-factorial and multi-step disease that involves chronic inflammation in every phase from initiation to progression and eventual plaque rupture.
In atherosclerosis, the endothelium's normal homeostatic functions are changed, facilitating an inflammatory response. For instance, inflamed endothelia express adhesion molecules. These adhesion molecules attract and recruit leukocytes, which subsequently move cross endothelial cells into the intima, making the vascular wall prone to lipid hyperplasia or vasculitis. Inflammatory mediators enhance the uptake of modified lipoprotein particles and the formation of lipid-filled macrophages. T cells also enter the intima and secrete cytokines, which further amplify the inflammatory response and promote the migration ＆ proliferation of intimal smooth muscle cells.
The inner membrane of a normal arterial wall is composed of a single layer of endothelial cells. The tiny gaps between the cells may allow the entry of HDL ＆ some of the smaller LDLD and VLDL into the arterial wall and the flux of a large amount of atherogenic lipoprotein into the blood. Under certain atherogenic factors such as inflammation or given vasoactive substances (e.g. bradykinin, histamine, catecholamine, serotonin, and prostaglandin E, etc.), endothelial cells suffer damage and contract, making the intercellular gaps increase. Numerous lipoprotein in the blood (except for the too large chylomicrons) will penetrate the intima of the artery, leading to the proliferation of intimal smooth muscle cells, increased synthesis of connective tissue and matrix components, and lipid deposition inside ＆ outside the cells. All these processes eventually induce the information of atherosclerotic plaque.
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