Skip to main content

CORRECTION article

Front. Pharmacol., 15 December 2021
Sec. Cardiovascular and Smooth Muscle Pharmacology

Corrigendum: C1q/TNF-Related Protein 9 Attenuates Atherosclerosis by Inhibiting Hyperglycemia-Induced Endothelial Cell Senescence Through the AMPKα/KLF4 Signaling Pathway

Gang Wang,Gang Wang1,2Baihe Han,Baihe Han1,2Ruoxi ZhangRuoxi Zhang3Qi Liu,Qi Liu1,2Xuedong Wang,Xuedong Wang1,2Xingtao Huang,Xingtao Huang1,2Dandan Liu,Dandan Liu1,2Weishen Qiao,Weishen Qiao1,2Mengyue Yang,Mengyue Yang1,2Xing Luo,Xing Luo1,2Jingbo Hou,
Jingbo Hou1,2*Bo Yu,Bo Yu1,2
  • 1The Key Laboratory of Myocardial Ischemia Organization, Chinese Ministry of Education, Harbin, China
  • 2Department of Cardiology Organization, The Second Affiliated Hospital of Harbin Medical University, Harbin, China
  • 3Department of Cardiology, Harbin Yinghua Hospital, Harbin, China

A corrigendum on
C1q/TNF-Related Protein 9 Attenuates Atherosclerosis by Inhibiting Hyperglycemia-Induced Endothelial Cell Senescence Through the AMPKα/KLF4 Signaling Pathway

by Wang, G., Han, B., Zhang, R., Liu, Q., Wang, X., Huang, X., Liu, D., Qiao, W., Yang, M., Luo, X., Hou, J., and Yu, B. (2021). Front. Pharmacol. 12:758792. doi: 10.3389/fphar.2021.758792

In the original article, there was a mistake in the artwork for Figure 2C as published. We made a careless mistake about p21 protein. The correct artwork appears below.

FIGURE 2
www.frontiersin.org

FIGURE 2. Hyperglycemia-induced HUVEC senescence is KLF4 dependent. (A) KLF4, as measured by immunoblotting and qRT-PCR in HUVECs after transfection with siNC or siKLF4 for 48 h. (B) Cells were fixed and stained for SA-β-gal activity and the histogram represents the percentage of SA-β-gal-positive cells per microscopic field. Values represent mean ± SEM. *p < 0.05, **p < 0.01. (C) KLF4, p21, and TERT protein levels were determined by immunoblotting. (D–F) Results were normalized to controls, and histograms represent the relative intensity of KLF4, p21, and TERT. Values represent mean ± SEM (n = 3–4 per group). *p < 0.05, **p < 0.01, ***p < 0.001.

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: CTRP9, atherosclerosis, senescence, hyperglycemia, AMPK, KLF4

Citation: Wang G, Han B, Zhang R, Liu Q, Wang X, Huang X, Liu D, Qiao W, Yang M, Luo X, Hou J and Yu B (2021) Corrigendum: C1q/TNF-Related Protein 9 Attenuates Atherosclerosis by Inhibiting Hyperglycemia-Induced Endothelial Cell Senescence Through the AMPKα/KLF4 Signaling Pathway. Front. Pharmacol. 12:812384. doi: 10.3389/fphar.2021.812384

Received: 10 November 2021; Accepted: 22 November 2021;
Published: 15 December 2021.

Edited and reviewed by:

Francesco Rossi, University of Campania Luigi Vanvitelli, Italy

Copyright © 2021 Wang, Han, Zhang, Liu, Wang, Huang, Liu, Qiao, Yang, Luo, Hou and Yu. 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: Jingbo Hou, amluZ2JvaG91QDE2My5jb20=

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.