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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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NOX4 mediates HKMT-induced EMT and intracellular ROS production via activation ERK signaling. PMCs were treated with HKMT in the presence or absence of the ERK inhibitor (PD98059). (a) Western blotting analyses of NOX4, phosphorylated ERK, collagen, and EMT markers. (b) Representative photomicrographs of cells subjected to DCFA–DA treatment * p < 0.05. Data are presented as the mean ± SD of three independent experiments. NOX, NADPH oxidase; EMT, epithelial to mesenchymal transition; COL1A, Collagen 1A.

NOX4 mediates HKMT-induced EMT and intracellular ROS production via activation ERK signaling. PMCs were treated with HKMT in the presence or absence of the ERK inhibitor (PD98059). (a) Western blotting analyses of NOX4, phosphorylated ERK, collagen, and EMT markers. (b) Representative photomicrographs of cells subjected to DCFA–DA treatment * p < 0.05. Data are presented as the mean ± SD of three independent experiments. NOX, NADPH oxidase; EMT, epithelial to mesenchymal transition; COL1A, Collagen 1A.