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. 2018 Mar 3;7(5):e007430. doi: 10.1161/JAHA.117.007430

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© 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Inwardly rectifying K⁺ (Kir) 2.1 deficiency promotes the formation and alters the distribution of atherosclerotic lesions in mouse aortas. A, Representative images of en face aortas from apolipoprotein E–deficient (Apoe ^−/−; left) and Kir2.1 ^+/− /Apoe ^−/− (right) stained with Oil Red O for lesion detection. Mice were fed a Western, high‐fat, high‐cholesterol diet (HFD) for 9 months before analysis. Aortas were isolated into the thoracic region immediately before the diaphragm. B, Group analyses of the lesions detected show lesion formation in the aortic arch (AA) and descending aorta (DA) as measured as percentage of the total area containing lesions. Larger, lower bars represent the group average and smaller, upper bars represent the standard error. For all groups, n=4. Significance was tested using 2‐way ANOVA. P<0.05 when comparing Apoe ^−/− and Kir2.1 ^+/− /Apoe ^−/−.