When there is too much inflammation in the body, the inner lining (endothelium) of the artery walls can become damaged. This causes the endothelial cells to produce various adhesion molecules that attract white blood cells and cause them to bind to the artery wall. The particular white blood cells that bind are monocytes and T lymphocytes. These blood cells migrate deep into the lining of the arteries. The monocytes turn into macrophages, which are a type of white blood cell that act like Ðàñ man; they engulf dead cells, bacteria and various debris. The macrophages start ingesting LDL cholesterol, and once they are filled with fat, they are referred to as foam cells. It is especially oxidized LDL particles that are ingested; these are particles that have been damaged by free radicals, either because of the way food has been processed, or because we do not have enough antioxidants in our body to prevent this. Oxidized LDL cholesterol also causes direct damage to the endothelium.
Inflammatory chemicals called cytokines are produced by the white blood cells that have entered the artery wall. These cytokines attract more white blood cells to the area and also stimulate the growth of smooth muscle cells of the artery wall. As smooth muscle cells accumulate, they cause the artery wall to thicken, which narrows the diameter of the artery. The smooth muscle cells produce enzymes that cause the breakdown of collagen and elastin in the artery wall. The macrophages also produce protein digesting enzymes that break down collagen. This makes the fatty plaque unstable and prone to rapture. If it raptures it is more likely to form a clot and block an artery completely. As atherosclerotic plaques progress, they tend to calcify, or harden because they accumulate calcium; this hardening is referred to as arteriosclerosis.
Damage to the endothelium also impairs the production of nitric oxide by cells lining the artery wall. Nitric oxide is your artery’s best friend because it dilates the arteries, has an anti inflammatory effect, and limits the ability of white blood cells to bind to the artery wall and initiate plaque formation.
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