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. 2019 Jul 12;8(14):e011994. doi: 10.1161/JAHA.119.011994

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© 2019 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ 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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Stress altered the levels of targeted protein in the injured arteries. A through C, Representative images and combined quantitative data for the levels of targeted proteins. Results are mean±SEM (n=5–7). AKT indicates protein kinase B; ATR1, angiotensin II receptor 1; CatS^+/+, cathepsin S wild type; Erk, extracellular signal‐regulated kinase; GSK, phosphoglycogene synthesis kinase; mTOR, mammalian target of rapamycin; NS, no significance; p‐AKT, phosphorylated AKT; p‐Erk, phosphorylated Erk; p‐mTOR, phosphorylated mTOR. ***P<0.001 vs the relative controls by 1‐way ANOVA, followed by Tukey post hoc tests.