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[Molecular mechanisms of coronary atherosclerotic plaque formation and rupture].

Rupture or erosion of atherosclerotic plaques of the coronary artery followed by thrombus formation appears to be the major causes of acute coronary syndrome. Rupture-prone vulnerable or unstable plaques have been proposed as those with thin fibrous caps, large lipid cores, and enhanced inflammatory responses as well as oxidative and mechanical stresses. Angiotensin II, oxidized low-density lipoprotein(LDL), and its receptor lectin-like oxidized LDL receptor-1(LOX-1) appear to play key roles in atherosclerotic plaque vulnerability and rupture. In addition soluble LOX-1 can be a biomarker for acute coronary syndrome reflecting plaque vulnerability and rupture.