Elucidation of molecular mechanism of plaque destabilization and identification of predictable factors for acute coronary syndrome

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We tried to elucidate molecular mechanism of plaque destabilization by analyzing clinical samples and utilizing animal models. The concentration of HMGB1, a non-histone nuclear protein, increased at coronary sinus in patients with coronary artery disease. Particularly, acute coronary syndrome, such as acute myocardial infarction or unstable angina pectoris, was associated with ten times elevated HMGB1 level. Animal experiments revealed that HMGB1-DNA complex signal contributed destabilization of vessel wall by activating Toll-like receptor 9 in the bone marrow-derived cells.