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. 2021 Mar 5;12(3):248. doi: 10.1038/s41419-021-03518-w

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© The Author(s) 2021

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 — Mice were treated with either Trametinib (1 mg/kg/d IP) or vehicle (3% DMSO in saline) for 3 days. Mice then underwent either no surgical manipulations (NORM), sham surgery (SHAM), or unilateral nephrectomy (UNX). Each mouse was treated with either vehicle (VEH) or BafA1 (BAF) and after 2 h the contralateral kidney was harvested. A pERK1/2 was significantly increased in sham surgery and UNX vs. normal kidneys. B Trametinib resulted in a near disappearance of pERK1/2 in sham surgery and UNX kidneys. C Trametinib resulted in a significant decrease in p62 in sham surgery and UNX kidneys compared to normal kidneys, but did not change the suppressed autophagic flux that was seen in sham surgery and UNX kidneys. Immunoblot analysis of LC3-II and p62 in the kidney with representative densitometry is demonstrated. RDU= relative densitometry units corrected for GAPDH. *P < 0.05, **P < 0.01, ***P < 0.001.