This article is a correction to:
C1q/TNF-Related Protein 9 Attenuates Atherosclerosis by Inhibiting Hyperglycemia-Induced Endothelial Cell Senescence Through the AMPKα/KLF4 Signaling Pathway
Gang Wang1,2
Baihe Han1,2
Ruoxi Zhang3Qi Liu1,2Xuedong Wang1,2Xingtao Huang1,2Dandan Liu1,2Weishen Qiao1,2Mengyue Yang1,2Xing Luo1,2Jingbo Hou1,2*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
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
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.
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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, ItalyCopyright © 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, jingbohou@163.com