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. 2019 Jan 23;9:323. doi: 10.1038/s41598-018-36911-1

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© The Author(s) 2019

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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A diagram depicting the proposed roles of AS-IV in hyperglycaemia-triggered podocyte EMT. In response to the harmful stimuli of high glucose, podocytes undergo EMT. During this state, SIRT1 expression is reduced, which further leads to the inhibition of deacetylation activity. The NF-kB subunit p65 enters the nucleus and is acetylated (AC-p65). The increased expression of AC-p65 leads to the decrease of autophagy. AS-IV treatment increases the expression of SIRT1, which leads to the increase of deacetylation activity. AC-p65 is consequently down-regulated, thus increasing levels of autophagy. Therefore, AS-IV can ameliorate podocyte EMT through enhancement of autophagy by SIRT1 deacetylation of the p65 subunit of NF-kB.