Studies of the pathophysiologic mechanism of both acute coronary syndromes and plaque stabilizing treatment are driving the development of animal models of vulnerable plaque. In contrast to advances in human studies of pathology, the definition, criteria and classification of vulnerable and ruptured plaques in animal models are still in dispute. Many approaches to increasing the intrinsic vulnerability of plaques or extrinsic forces on plaques have been reported. However, an ideal animal model mimicking human plaque rupture is still lacking, and the exact cellular and molecular mechanisms of plaque progression are not fully understood. This review summarizes current progress in animal model studies related to plaque destabilization and disruption and the possible mechanisms involved.
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