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CORRECTION article

Front. Physiol., 06 February 2020
Sec. Vascular Physiology
Volume 11 - 2020 | https://doi.org/10.3389/fphys.2020.00059

Corrigendum: Propofol Alleviates DNA Damage Induced by Oxygen Glucose Deprivation and Reperfusion via FoxO1 Nuclear Translocation in H9c2 Cells

This article is a correction to:

  1. Propofol Alleviates DNA Damage Induced by Oxygen Glucose Deprivation and Reperfusion via FoxO1 Nuclear Translocation in H9c2 Cells

    1. Read original article
\nDandan Zhou&#x;Dandan Zhou1†Jinqiang Zhuang&#x;Jinqiang Zhuang1†Yihui WangYihui Wang1Dandan ZhaoDandan Zhao1Lidong ZhaoLidong Zhao1Shun Zhu,Shun Zhu1,2Jinjun PuJinjun Pu3Ming YinMing Yin2Hongyu ZhangHongyu Zhang4Zejian Wang Zejian Wang2*Jiang Hong Jiang Hong1*
  • 1Department of Internal and Emergency Medicine, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China
  • 2School of Pharmacy, Shanghai Jiao Tong University, Shanghai, China
  • 3Department of Emergency Medicine, Putuo Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China
  • 4Department of Biomedicine, KG Jebsen Centre for Research on Neuropsychiatric Disorders, University of Bergen, Bergen, Norway

A Corrigendum on
Propofol Alleviates DNA Damage Induced by Oxygen Glucose Deprivation and Reperfusion via FoxO1 Nuclear Translocation in H9c2 Cells

by Zhou, D., Zhuang, J., Wang, Y., Zhao, D., Zhao, L., Zhu, S., et al. (2019). Front. Physiol. 10:223. doi: 10.3389/fphys.2019.00223

In the original article, there was a mistake in Figure 6 as published. In Part A, the images of IRS-1 and p-IRS-1 were the same as the images of AMPK and p-AMPK. The corrected Figure 6 appears below.

FIGURE 6
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Figure 6. Propofol inhibited FoxO1 phosphorylation through Akt and AMPK pathways. (A) The expression of proteins in FoxO1-related pathways in H9c2 cells. (B) The expression of p-FoxO1 after being treated with inhibitors and activators of Akt and AMPK pathways. (C) Cell viability was assessed by MTT assay after FoxO1 siRNA transfection in H9c2 cells. (D–E) Cell viability was assessed by MTT assay after being treated with inhibitors and activators of Akt and AMPK pathways. The data are presented as the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 versus control, #p < 0.05, ##p < 0.01, ###p < 0.001 versus OGD/R treated group without drugs.

The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.

Keywords: propofol, oxygen glucose deprivation and reperfusion, ROS, DNA damage, FoxO1

Citation: Zhou D, Zhuang J, Wang Y, Zhao D, Zhao L, Zhu S, Pu J, Yin M, Zhang H, Wang Z and Hong J (2020) Corrigendum: Propofol Alleviates DNA Damage Induced by Oxygen Glucose Deprivation and Reperfusion via FoxO1 Nuclear Translocation in H9c2 Cells. Front. Physiol. 11:59. doi: 10.3389/fphys.2020.00059

Received: 18 December 2019; Accepted: 21 January 2020;
Published: 06 February 2020.

Edited and reviewed by: Tommaso Angelone, Università della Calabria, Italy

Copyright © 2020 Zhou, Zhuang, Wang, Zhao, Zhao, Zhu, Pu, Yin, Zhang, Wang and Hong. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Zejian Wang, wangzejian@sjtu.edu.cn; Jiang Hong, jhong.pku@163.com

†These authors have contributed equally to this work

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.