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. 2020 May 21;10:8418. doi: 10.1038/s41598-020-65423-0

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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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Modulation of SIRT3 preserves mitochondria ultrastructure and homeostasis in podocytes. (a) Representative electron microscopy images of podocytes from BTBR WT mice and from BTBR ob/ob mice treated with vehicle or honokiol at 14 weeks of age. Scale bars: 2 μm. (b) Enlarged images show mitochondria structure in podocytes of WT and diabetic mice. Scale bars: 500 nm. (c) Representative images and quantification of glomerular PGC-1α expression in BTBR WT mice (n = 9) and in BTBR ob/ob mice treated with vehicle (n = 6) and honokiol (n = 9) at 14 weeks of age. Honokiol increases the percentage of PGC-1α-positive nuclei in diabetic mice (arrowheads and insets). Scale bars: 20 μm. Data are mean ± SEM and were analyzed by one-way ANOVA followed by Tukey’s multiple comparisons test, ***p < 0.001 vs BTBR WT mice; ^##p < 0.01 vs BTBR ob/ob + vehicle.