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. 2020 Feb 6;11(2):96. doi: 10.1038/s41419-020-2296-4

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© The Author(s) 2020

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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Fig. 6 — a, b Protein levels of IGF1R, PI3K, AKT1 in NRCMs treated with mCRAMP (0.5 mg/L) and Ang II (1 μM) (n = 6). *P < 0.05 vs. vehicle-CON; ^#P < 0.05 vs. vehicle-Ang II. c, d Protein levels of IGF1R, PI3K, AKT1 in remodeling heart tissue treated with mCRAMP (n = 6, *P < 0.05 vs. CON-sham; ^#P < 0.05 vs. CON-AB). e–i NRCMs were transfected with AKT1 siRNA and treated with mCRAMP (0.5 mg/L) and Ang II (1 μM). e Protein levels of AKT1 in NRCMs (n = 6). f, g α-actin staining (n = 6) and cell surface area (n > 50 cells per group). h ROS levels (n = 6). *P < 0.05 vs. CON; ^#P < 0.05 vs. Ang II. i Co-IP experiment in NRCMs.