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An essential role for Wnt/β-catenin signaling in mediating hypertensive heart disease by Zhao, Yue; Wang, Chunhong; Wang, Cong; Hong, Xue; Miao, Jinhua; Liao, Yulin; Zhou, Lili; Liu, Youhua is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.
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## Abstract Activation of the renin-angiotensin system (RAS) is associated with hypertension and heart disease. However, how RAS activation causes cardiac lesions remains elusive. Here we report the involvement of Wnt/β-catenin signaling in this process. In rats with chronic infusion of angiotensin II (Ang II), eight Wnt ligands were induced and β-catenin activated in both cardiomyocytes and cardiac fibroblasts. Blockade of Wnt/β-catenin signaling by small molecule inhibitor ICG-001 restrained Ang II-induced cardiac hypertrophy by normalizing heart size and inhibiting hypertrophic marker genes. ICG-001 also attenuated myocardial fibrosis and inhibited α-smooth muscle actin, fibronectin and collagen I expression. These changes were accompanied by a reduced expression of atrial natriuretic peptide and B-type natriuretic peptide. Interestingly, ICG-001 also lowered blood pressure induced by Ang II. In vitro, Ang II induced multiple Wnt ligands and activated β-catenin in rat primary cardiomyocytes and fibroblasts. ICG-001 inhibited myocyte hypertrophy and Snail1, c-Myc and atrial natriuretic peptide expression, and abolished the fibrogenic effect of Ang II in cardiac fibroblasts. Final
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- Author
- Zhao, Yue; Wang, Chunhong; Wang, Cong; Hong, Xue; Miao, Jinhua; Liao, Yulin; Zhou, Lili; Liu, Youhua
- Publisher
- Springer Science and Business Media LLC; London: Nature Publishing Group; [London]: Springer Nature; Nature Publishing Group; Society for Mining, Metallurgy and Exploration Inc.; Research Square; Springer Nature; Island Press (ISSN 2045-2322)
- Published
- 2018
- Language
- EN
- Field
- Biochemistry, Genetics and Molecular Biology (Life Sciences)