Among the most common models in atherosclerosis research is the atherosclerosis-prone mouse. Genetically manipulated mouse strains such as the ApoE−/− mouse will reliably form plaques under certain conditions, and these lesions have been noted to exhibit morphological and biochemical similarities with human atherosclerotic plaques. Unlike plaques in humans, however, murine plaques are not observed to rupture and form occlusive thrombi [1]. As atherosclerosis and its complications are the leading cause of death in the modern world, a comprehensive understanding of the mechanisms of plaque disruption is essential to develop diagnostic and interventional techniques. Although the mouse model is frequently employed to study plaque formation, its validity for studying plaque disruption events such as rupture or erosion has been questioned.

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