The rupture of atherosclerotic plaques induces the formation of clots that block blood supply to the heart or brain, which can precipitate heart attack or stroke, respectively. Existing models of atherogenesis such as ApoE−/− mice lack several features present in the human vulnerable plaque. Now, Najafi, Aghili et al. report that lard-fed mixed-background ApoE−/− mice exposed to chronic stress develop inflamed atherosclerotic lesions with a large necrotic core and a thin fibrous cap. Notably, neovascularisation and intraplaque haemorrhage develop in most of these animals by 20 weeks of age. This new model should facilitate the investigation of the mechanisms underlying the formation of vulnerable atherosclerotic plaques, and the development of therapeutic interventions that affect both plaque vulnerability and plaque burden. Page 323

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