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. 2020 Feb 3;11(2):87. doi: 10.1038/s41419-020-2275-9

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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. 7 — Autophagic activity seems to upregulate when RAS is overexpressed. The key player of RAS (1) Ang II induces autophagy via AT1 receptor whereas (2) the interaction of Ang II with AT2 receptor attenuates autophagic function in cardiomyocytes and in neuronal cells. In addition, (3) Ang 1–7 provides a protective function by downregulating autophagy. However, (4) some evidence shows that Ang 1–7 does not inhibit autophagy but induces it via induced cofilin-1 expression. The role of Ang (1–7) on autophagy is controversial and more research is required to understand the underlining mechanisms. Upregulation of autophagy due to RAS overexpression could be via NOX and ROS production. Nevertheless, the underlying mechanisms are yet to be identified.