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. 2017 Apr 6;7:672. doi: 10.1038/s41598-017-00796-3

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© The Author(s) 2017

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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Model of PGC-1α/NRF2-Sirt3 pathway in regulating NaF-induced nephrotoxicity. PGC-1a interacts with NRF2 as a transcriptional coactivator and its reduction decreases Sirt3 transcription. A reduction in Sirt3 decreases the deacetylation of FoxO3a and SOD2, resulting in ROS accumulation. Increased ROS level activates ERK1/2, resulting in cellular apoptosis.