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. 2019 Jan 18;8(1):116. doi: 10.3390/jcm8010116

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Toll like receptor 4 (TLR4) inhibition and angiotensin II receptor type1 (AT1R) inhibition reduce HKMT-induced NOX–ROS production and collagen synthesis. (a) Western blotting analyses of NOX4, phosphorylated ERK, collagen, and EMT markers. (b) Collagen-1 mRNA concentration by RT-PCR. (c) Representative photomicrographs of cells subjected to DCFA–DA treatment. Data are presented as the mean ± SD of three independent experiments.* p < 0.05. Losartan, AT1 receptor antagonist; TAK242, NOX: NADPH oxidase; EMT, epithelial to mesenchymal transition; COL1A, Collagen 1A.

Toll like receptor 4 (TLR4) inhibition and angiotensin II receptor type1 (AT1R) inhibition reduce HKMT-induced NOX–ROS production and collagen synthesis. (a) Western blotting analyses of NOX4, phosphorylated ERK, collagen, and EMT markers. (b) Collagen-1 mRNA concentration by RT-PCR. (c) Representative photomicrographs of cells subjected to DCFA–DA treatment. Data are presented as the mean ± SD of three independent experiments.* p < 0.05. Losartan, AT1 receptor antagonist; TAK242, NOX: NADPH oxidase; EMT, epithelial to mesenchymal transition; COL1A, Collagen 1A.