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Atherosclerosis is a disorder of the arteries characterized by the formation of hard structures called atherosclerotic plaques. It is a prevalent disorder, accounting for one third of all deaths in North America.
Formation of atherosclerotic plaques is a progressive process and the exact cause is unknown but it is believed to originate from damage to the arterial wall. One possible cause of this damage is oxidized low-density lipoprotein (LDL). Initially a 'fatty streak' forms in the artery wall, which damages the blood vessel and initiates an inflammatory process. Monocytes invade the artery wall and differentiate into macrophages. Macrophages absorb the oxidized low density lipoproteins (LDL), form 'foam cells' and develop into a 'fatty streak'. Foam cells are unable to process oxidized-LDL and they ultimately grow and rupture, depositing more oxidized-LDL into the artery wall, causing the invasion of more macrophages and propagating the inflammatory response. Eventually muscle cells enlarge and form a fibrous cap over the fatty plaque, resulting in narrowing of the artery. The fibrous cap is prone to rupture and subsequent exposure of the plaque core leads to acute thrombus formation and myocardial infarction.
Risk factors for the development of atherosclerosis include hyperlipidemia, hypertension, diabetes, male gender and advanced age. Current treatment options comprise the cholesterol lowering drugs statins and surgical intervention. New pharmacological targets include PPAR, cytokines, matrix metalloproteases and adhesion molecules.