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. 2018 Apr 19;8:6277. doi: 10.1038/s41598-018-24749-6

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© The Author(s) 2018

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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Hyperthermia treatment prevented fibrotic change in angiotensin infusion model. (a) Picture of mice undergoing hyperthermia treatment by heating plate. (b) Ang II increased systolic blood pressure (SBP) in mice with or without hyperthermia (normal saline (NS), Ang II infusion (AT) and Ang II infusion with hyperthermia treatment (AT + heat)), (n = 5, ***p < 0.001, ns: no significant difference). (c) Sirius Red staining of heart sections. Scale bars: 600 μm (top), 100 μm (bottom). Representative images of perivascular fibrosis (left) and quantitative analysis of fibrotic area in left ventricle (LV) (right, n = 4–5, ***p < 0.001). (d) Hyperthermia attenuated α-SMA mRNA expression in mice LV (n = 5, *p < 0.05). (e) Immunohistological staining of heart sections for α-SMA (brown). Scale bars: 100 μm. (n = 4, *p < 0.05, **p < 0.01).