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. 2020 Jul 21;11(7):554. doi: 10.1038/s41419-020-02765-7

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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–c Autophagy inducer rapamycin attenuated cardiac injury induced by p21 downregulation. Relative mRNA level of TNFα, SOD2, and NOX2 in the indicated groups of NRCMs (a, n = 6). Representative western blot analysis of p-mTOR, mTOR, LC3B, p62, and GAPDH in NRCMs (b, n = 6). Cardiac EF was measured by echocardiography in the indicated mouse hearts (c, n = 6). d, e p21 overexpression activated autophagy flux and attenuated inflammation and oxidative stress induced by LPS. Representative western blot analysis of p21, LC3, p62, and GAPDH in NRCMs (d, n = 6) and relative mRNA levels of TNFα and SOD2 in NRCMs (e, n = 6). *p < 0.05 versus Ctrl group, ^#p < 0.05 versus corresponding LPS group.