CORRECTION article

Front. Bioeng. Biotechnol., 02 November 2022

Sec. Tissue Engineering and Regenerative Medicine

Volume 10 - 2022 | https://doi.org/10.3389/fbioe.2022.1045496

Corrigendum: Activation of the NFκB signaling pathway in IL6+CSF3+ vascular endothelial cells promotes the formation of keloids

  • 1. Department of General Surgery, Institute for Minimally Invasive Surgery, Affiliated Zhongda Hospital, Medical School, Southeast University, Nanjing, China

  • 2. Department of Endocrinology, Affiliated Zhongda Hospital, Medical School, Southeast University, Nanjing, China

  • 3. School of Statistics, Renmin University of China, Beijing, China

  • 4. Beijing Sankuai Online Technology Co., Ltd., Dhaka, Bangladesh

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In the published article, there was an error in affiliations [1, 2]. Instead of

1Department of General Surgery, Institute for Minimally Invasive Surgery, Affiliated ZhongDa Hospital, Medical School, Southeast University, Dhaka, Bangladesh

2Department of Endcrinology, Affiliated ZhongDa Hospital, Medical School, Southeast University, Dhaka, Bangladesh, it should be

1Department of General Surgery, Institute for Minimally Invasive Surgery, Affiliated ZhongDa Hospital, Medical School, Southeast University, Nanjing, China

2Department of Endcrinology, Affiliated ZhongDa Hospital, Medical School, Southeast University, Nanjing, China”

In the published article, there was an error regarding the affiliation(s) for Delin Liu. As well as having affiliation “1”, they should also have “Department of Endcrinology, Affiliated Zhongda Hospital, Medical School, Southeast University, Nanjing, China”.

A correction has been made to Results, The endothelial cells of keloid are divided into four subgroups, [176–180]. This sentence previously stated:

“genes upregulated in Endo1 were mainly involved in Osteoclast differentiation, TNF signaling Endo1 upregulated genes were mainly involved in Osteoclast differentiation, TNF signaling pathway, Apoptosis; Endo2 upregulated genes were mainly involved in IL-17 signaling pathway, Fluid shear stress and atherosclerosis, Rheumatoid arthritis; Endo3 upregulated genes were mainly involved in Endo3 upregulated genes are mainly involved in Endocrine resistance, Estrogen signaling pathway, Proteoglycans in cancer and other signaling pathways”

The corrected sentence appears below:

“genes upregulated in Endo1 were mainly involved in Osteoclast differentiation, TNF signaling pathway, Apoptosis; Endo2 upregulated genes were mainly involved in IL-17 signaling pathway, Fluid shear stress and atherosclerosis, Rheumatoid arthritis; Endo3 upregulated genes were mainly involved in Endocrine resistance, Estrogen signaling pathway, Proteoglycans in cancer and other signaling pathways”

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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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.

Summary

Keywords

keloid, IL6, endothelial cells (ECs), scRNAseq, NFkB (RelA)

Citation

Liu D, Zhang Y, Zhen L, Xu R, Ji Z and Ye Z (2022) Corrigendum: Activation of the NFκB signaling pathway in IL6+CSF3+ vascular endothelial cells promotes the formation of keloids. Front. Bioeng. Biotechnol. 10:1045496. doi: 10.3389/fbioe.2022.1045496

Received

15 September 2022

Accepted

20 September 2022

Published

02 November 2022

Approved by

Frontiers Editorial Office, Frontiers Media SA, Switzerland

Volume

10 - 2022

Updates

Copyright

*Correspondence: Zhenling Ji, ; Zheng Ye,

This article was submitted to Tissue Engineering and Regenerative Medicine, a section of the journal Frontiers in Bioengineering and Biotechnology

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.

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