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. 2017 Jan 5;113(3):276–287. doi: 10.1093/cvr/cvw258

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© The Author 2017. Published by Oxford University Press on behalf of the European Society of Cardiology

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Tipifarnib attenuates development of chronic hypoxia-induced pulmonary hypertension. (A) right ventricular hypertrophy (RVH), (B) Right ventricular systolic pressure (RVSP), (C, D) vessel muscularization in the lungs of normoxic and chronically hypoxic mice treated with vehicle or tipifarnib (100 mg/kg). In (D) top panel shows smooth muscle actin (SMA) staining in lung sections from hypoxic control lungs and bottom panel shows SMA staining in lungs from tipifarnib-treated hypoxic mice. Magnified boxed areas illustrate changes in muscularization of small intrapulmonary arteries. In (A–C) values are means ± SEM of n = 6; *P < 0.05, **P < 0.01, ***P < 0.001 vs. normoxic control; ^##P < 0.01, ^###P < 0.001 vs. hypoxic control. 1-way ANOVA with Tukey post-test.