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. 2018 Jan 22;25(5):966–982. doi: 10.1038/s41418-017-0036-9

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, and provide a link to the Creative Commons license. You do not have permission under this license to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/.

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Fig. 3 — a The levels of YAP/TAZ in the myocardium are greater in P1 and P3 neonatal mice and are gradually decreased in P7, P14 and P21 neonatal mice. b, c Increased YAP levels in neonatal cardiomyocytes by transfection of AAV virus expressing activated YAP1 increased YAP1 levels (B) and promoted neonatal cardiomyocyte proliferation c. d-f Inhibition of YAP1 expression by specific siRNA for YAP1 or YAP inhibitor, verteporfin (VP) markedly suppressed Poly I:C (PIC)-induced neonatal cardiomyocyte proliferation d, YAP1 expression in cytosol e, f and nuclear translocation g. n = 3–8/group. *p < 0.05 compared with indicated groups. ^#p < 0.05 compared with the control group