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CORRECTION article

Front. Pharmacol., 19 July 2024
Sec. Experimental Pharmacology and Drug Discovery
Volume 15 - 2024 | https://doi.org/10.3389/fphar.2024.1451696

Corrigendum: Ginsenoside Re attenuates high glucose-induced RF/6A injury via regulating PI3K/AKT inhibited HIF-1a/VEGF signaling pathway

This article is a correction to:

  1. Corrigendum: Ginsenoside Re Attenuates High Glucose-Induced RF/6A Injury via Regulating PI3K/AKT Inhibited HIF-1a/VEGF Signaling Pathway

    1. Read original article
Weijie Xie&#x;Weijie Xie1†Ping Zhou&#x;Ping Zhou1†Muwen QuMuwen Qu2Ziru DaiZiru Dai1Xuelian ZhangXuelian Zhang1Chenyang ZhangChenyang Zhang1Xi DongXi Dong1Guibo Sun Guibo Sun1*Xiaobo Sun Xiaobo Sun1*
  • 1Institute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China
  • 2Guang’anmen Hospital, Chinese Academy of Chinese Medical Sciences, Beijing, China

A Corrigendum on
Ginsenoside Re attenuates high glucose-induced RF/6A injury via regulating PI3K/AKT inhibited HIF-1a/VEGF signaling pathway

by Xie W, Zhou P, Qu M, Dai Z, Zhang X, Zhang C, Dong X, Sun G and Sun X (2020). Front. Pharmacol. 11:695. doi: 10.3389/fphar.2020.00695

In the original article, there was a mistake in the Figure 7 as published. The protein band of β-actin in Figure 7B were misplaced. The corrected Figure 7 and its caption appears below.

Figure 7
www.frontiersin.org

Figure 7. Re protects RF/6A cells via regulation of the PI3K/Akt pathway. (A), Akt and p-AKT expression detected by western blot. (B), The changes of related proteins after LY294002 (PI3K inhibitor) incubation. (C), Analysis of Akt and p-Akt expression. (D–H), Statistic analysis of related protein levels. The results are presented as the mean ± SEM percentage of the control from three independent tests. ##p < 0.01 versus the control group; *p < 0.05, **p < 0.01 versus the HG group.

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.

Publisher’s note

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.

Keywords: ginsenoside Re, diabetic retinopathy, oxidative stress, apoptosis, phosphoinositide 3-kinase/AKTT, hypoxia-inducible factor-1-alpha, vascular endothelial growth factor

Citation: Xie W, Zhou P, Qu M, Dai Z, Zhang X, Zhang C, Dong X, Sun G and Sun X (2024) Corrigendum: Ginsenoside Re attenuates high glucose-induced RF/6A injury via regulating PI3K/AKT inhibited HIF-1a/VEGF signaling pathway. Front. Pharmacol. 15:1451696. doi: 10.3389/fphar.2024.1451696

Received: 19 June 2024; Accepted: 02 July 2024;
Published: 19 July 2024.

Edited and reviewed by:

Wei Peng, Chengdu University of Traditional Chinese Medicine, China

Copyright © 2024 Xie, Zhou, Qu, Dai, Zhang, Zhang, Dong, Sun and Sun. 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: Guibo Sun, c3VuZ3VpYm9AMTI2LmNvbQ==; Xiaobo Sun, c3VueGlhb2JvcGFwZXJAMTYzLmNvbQ==

†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.