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Atherosclerosis, or plaque buildup and immune cell infiltration into the arterial walls, is the most common pathological process leading to cardiovascular disease. The most widely used mouse models to delineate the mechanisms underlying atherosclerosis involve the genetic deletion of low-density lipoprotein receptor (Ldlr) or apolipoprotein E (ApoE). Recent data suggest that the environmental conditions ubiquitously employed in mouse housing lead to profound physiological alterations.

Giles, Ramkhelawon, and colleagues confirm previous reports that housing mice at their thermoneutral zone (TN, 29-32 °C) in combination with Western diet (WD) profoundly augments obesity development and promotes atherosclerosis in ApoE-/- mice. They show for the first time that TN housing in combination with WD promotes mild induction of atherosclerosis in wild-type (WT) mice as well. This increased disease burden is associated with altered cholesterol levels and fractions, augmented lipid profiles, and increased aortic plaque sizes. Further, the initiation of atherosclerosis in WT mice is accompanied with increased aortic and adipose tissue expression of inflammatory genes known to play a role in atherosclerosis and increased circulating immune cell expression of pathways related to adverse cardiovascular outcome.

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In this section authors briefly report on their work recently published in Molecular Metabolism.

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Randy J. Seeley, Henriette Frikke-Schmidt
Department of Surgery, University of Michigan, Ann Arbor, USA
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