Spontaneous Atherothrombosis and Medial Degradation in <i>Apoe</i> ^−/− , <i>Npc1</i> ^−/− Mice

Abstract

A defect in intracellular cholesterol trafficking caused by the Npc1 null mutation predisposes to increased lesion formation, atherothrombosis, and medial degradation. Plaque complications may require a procoagulant state and an increased protease activity, leading to plaque destabilization.