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CORRECTION article

Front. Pharmacol., 01 November 2022
Sec. Renal Pharmacology
Volume 13 - 2022 | https://doi.org/10.3389/fphar.2022.1022539

Corrigendum: Receptor of advanced glycation end products deficiency attenuates cisplatin-induced acute nephrotoxicity by inhibiting apoptosis, inflammation and restoring fatty acid oxidation

This article is a correction to:

  1. Receptor of Advanced Glycation End Products Deficiency Attenuates Cisplatin-Induced Acute Nephrotoxicity by Inhibiting Apoptosis, Inflammation and Restoring Fatty Acid Oxidation

    1. Read original article
Qiang Wang,Qiang Wang1,2Yuemei Xi,Yuemei Xi1,2Binyang Chen,Binyang Chen1,2Hairong Zhao,Hairong Zhao1,2Wei Yu,Wei Yu1,2De Xie,De Xie1,2Weidong Liu,Weidong Liu1,2Furong He,Furong He1,2Chenxi Xu,Chenxi Xu1,2Jidong Cheng, Jidong Cheng1,2*
  • 1Department of Internal Medicine, Xiang’an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China
  • 2Xiamen Key Laboratory of Translational Medicine for Nucleic Acid Metabolism and Regulation, Xiamen, China

A Corrigendum on
Receptor of advanced glycation end products deficiency attenuates cisplatin-induced acute nephrotoxicity by inhibiting apoptosis, inflammation and restoring fatty acid oxidation

by Wang Q, Xi Y, Chen B, Zhao H, Yu W, Xie D, Liu W, He F, Xu C and Cheng J (2022). Front. Pharmacol. 13:907133. doi: 10.3389/fphar.2022.907133

In the published article, there was an error in affiliation 1. Instead of “Department of Endocrinology, Xiang’an Hospital of Xiamen University, Xiamen, China”, it should be “Department of Internal Medicine, Xiang’an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China”.

In the published article, the reference Elimam et al. was not cited. The citation has now been inserted in Discussion, Paragraph 6, and now reads:

“Apart from being a source of energy, fatty acids are also engaged in the formation of mitochondrial membrane phospholipids. Calcium-independent Phospholipase A2γ can repair damaged mitochondrial membrane phospholipids by hydrolyzing damaged acyl chains to make them re-esterify with fatty acids and thus maintain mitochondrial survival and function, including FAO (Elimam et al., 2013).”

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.

Reference

Elimam, H., Papillon, J., Takano, T., and Cybulsky, A. V. (2013). Complement-mediated activation of calcium-independent phospholipase A2γ: Role of protein kinases and phosphorylation. J. Biol. Chem. 288 (6), 3871–3885. doi:10.1074/jbc.M112.396614

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Keywords: rage, cisplatin-induced nephrotoxicity, apoptosis, inflammation, fatty acid oxidation

Citation: Wang Q, Xi Y, Chen B, Zhao H, Yu W, Xie D, Liu W, He F, Xu C and Cheng J (2022) Corrigendum: Receptor of advanced glycation end products deficiency attenuates cisplatin-induced acute nephrotoxicity by inhibiting apoptosis, inflammation and restoring fatty acid oxidation. Front. Pharmacol. 13:1022539. doi: 10.3389/fphar.2022.1022539

Received: 18 August 2022; Accepted: 19 October 2022;
Published: 01 November 2022.

Approved by:

Frontiers Editorial Office, Frontiers Media SA, Switzerland

Copyright © 2022 Wang, Xi, Chen, Zhao, Yu, Xie, Liu, He, Xu and Cheng. 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: Jidong Cheng, amlkb25nY2hlbmczNkBob3RtYWlsLmNvbQ==

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.