Myocardial infarction is caused by rupture of the fibrous cap, with exposure of the lipid-rich core, or erosion, resulting in subsequent thrombosis and vessel occlusion. Plaques consist of a vascular smooth muscle cell (VSMC)-rich, fibrous cap, composed of collagen and extracellular matrix, which separates a lipid-rich core from the lumen. Our research studies the regulation of cell accumulation and interactions in vascular disease, using both human and mouse cells in vitro and models of atherosclerosis with genetic manipulation. We also have a major interest in vulnerable plaque imaging in patients using both invasive and non-invasive modalities.
Gray, K, Kumar, K, Figg, N, Harrison, J, Baker, L, Mercer, J, Littlewood, TD, Bennett, MR. Effects of DNA damage in smooth muscle cells in atherosclerosis. Circ Res 2015. In press.
Patel, MN, Bernard, WG, Milev, NB, Figg, N, Hart, D, Cawthorn, WB, Virtue, S, Hegyi, K, Chu, Y, Griffin, JL, Akira, S, Vidal-Puig, AJ, Bennett, MR, Sethi, JK. Hematopoietic IκB kinase epsilon limits NLRP3 inflammasome priming, metabolic disease progression and atherosclerosis. Proc Natl Acad Sci USA 2015;112(2):506-11
Teng, Z, Brown, AJ, Calvert, PA, Parker, RA, Obaid, DR, Huang, Y, Hoole, SP, West, NEJ, Gillard, J, Bennett, MR. Coronary plaque structural stress is determined by plaque composition and subtype and increased in acute coronary syndrome: the BEACON I (Biomechanical Evaluation of Atheromatous COroNary Arteries) Study. Circulation Cardiovascular Imaging. 2014. 101; 513-521.