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. 2017 May 15;7:1906. doi: 10.1038/s41598-017-01936-5

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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BNIP3L expression was up-regulated by the NE-AR-PKC signaling pathway. (a) Western blot analysis showing the effects of doxazosin (DOX) and metoprolol (MET) on AAC-induced BNIP3L. (b) Western blot analysis showing the effects of propranolol (PRO), phenoxybenzamine (PHE) and bisindolylmaleimide I (BIM) on NE-induced BNIP3L expression. (c) Western blot analysis showing the effects of DOX and MET on AAC-induced fibronectin expression. (d) Masson’s trichrome staining showing the effects of DOX and MET on AAC-induced cardiac fibrosis (*P < 0.05 vs. sham, ^#P < 0.05 vs. AAC). (e) Echocardiographic assessment showing the effects of DOX and MET on AAC-induced cardiac dysfunction (n = 8, *P < 0.05 vs. sham, ^#P < 0.05 vs. AAC).