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CORRECTION article

Front. Pharmacol., 10 October 2025

Sec. Renal Pharmacology

Volume 16 - 2025 | https://doi.org/10.3389/fphar.2025.1710281

Correction: Post-translational modifications in sepsis-induced acute kidney injury: mechanisms and perspectives

This article is a correction to:

  1. Post-translational modifications in sepsis-induced acute kidney injury: mechanisms and perspectives

    1. Read original article
Lin Song,&#x;Lin Song1,2†Wei Jiang,&#x;Wei Jiang1,2†Ke LiuKe Liu3Jing Wang,Jing Wang1,2Weilei GongWeilei Gong4Jiangquan Yu, Jiangquan Yu1,2*Ruiqiang Zheng, Ruiqiang Zheng1,2*
  • 1Northern Jiangsu People’s Hospital Affiliated to Yangzhou University, Yangzhou, China
  • 2Intensive Care Unit, Northern Jiangsu People’s Hospital, Yangzhou, China
  • 3Yangzhou University Hospital, Yangzhou, China
  • 4School of Pharmaceutical Sciences and Institute of Materia Medica, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, China

A Correction on
Post-translational modifications in sepsis-induced acute kidney injury: mechanisms and perspectives

by Song L, Jiang W, Liu K, Wang J, Gong W, Yu J and Zheng R (2025). Front. Pharmacol. 16:1625139. doi: 10.3389/fphar.2025.1625139

There was a mistake in the order of the Figures 2–5 as published. The figures and their corresponding figure captions for these results were all misaligned. The corrected figures and their captions appear below.

Figure 2
Diagram illustrating the inflammatory pathway initiated by Gram-negative bacteria. LPS from bacteria activates TLR4, leading to a cascade involving p38 MAPK, STAT3, IκBα, and NF-κB P65. This triggers pathways resulting in NO, ROS production, and Fis1 activity affecting mitochondria, with calpain activation related to inflammation.

Figure 2. Pathogenesis associated with Phosphorylation and sepsis-induced acute kidney injury. A significant production of inflammatory cytokines occurs within the glomeruli and renal tubular interstitium. The interaction between TLR4 and LPS activates the phosphorylation of P38 MAPK and NF-κB, while Lyn inhibits the phosphorylation of STAT3, thereby diminishing levels of inflammatory mediators. Moreover, the suppression of calpain activation can curtail P38 phosphorylation, reduce ROS, and consequently mitigate endothelial cell apoptosis. Additionally, DNA-PKcs can induce the phosphorylation of Fis1, resulting in mitochondrial dysfunction and subsequent cell apoptosis.

Figure 3
Diagram illustrating the molecular pathways involving CD36, BAP1, BRCA1, FOXQ1, USP10, SIRT6, and NRF2. CD36 interacts with Fis1 and affects mitochondria, leading to apoptosis. BAP1, BRCA1, and FOXQ1 influence NF-kB P65, causing inflammation. USP10 and SIRT6 interact, leading to NRF2 activation and affecting ROS levels. Each molecule and interaction is depicted with arrows, demonstrating the flow and impact on apoptosis, inflammation, and reactive oxygen species (ROS).

Figure 3. Pathogenesis associated with ubiquitination and sepsis-induced acute kidney injury. CD36 promotes ferroptosis in proximal tubular cells by regulating the ubiquitination of FSP1. The interaction between BAP1 and BRCA1 enhances the stability of BRCA1 protein through deubiquitination, thereby inhibiting NF-κB. Furthermore, FOXQ1, deubiquitinated by USP10, ameliorates cellular inflammation and apoptosis. Additionally, USP10 interacts with SIRT6 to suppress its ubiquitination, alleviating oxidative stress.

Figure 4
Diagram illustrating cellular processes with three main pathways. SIRT1 influences HMGB1, leading to apoptosis. SIRT3 interacts with TFAM and DNA-PKcs in a mitochondrion, affecting inflammation. P53, acetylated, is involved in autophagy.

Figure 4. Pathogenesis associated with acetylation and sepsis-induced acute kidney injury. The sirtuin family comprises the most prevalent deacetylases, with SIRT1 mediating the acetylation of HMGB1 and SIRT3 facilitating the acetylation of TFAM. Moreover, elevated levels of acetylated P53 in RTECs hinder autophagy.

Figure 5
Diagram illustrating lactate's effect on cellular processes. Increased lactate levels influence H3K18a, activating RhoA, and affect mitochondria via Lac and Fis1. This leads to apoptosis and inflammation.

Figure 5. Pathogenesis associated with lactylation and sepsis-induced acute kidney injury. In SA-AKI, elevated levels of lactate and histone lactylation, particularly the increased lactylation of H3K18, activate RhoA protein, thereby triggering inflammation and apoptosis. Additionally, lactate mediates the lactylation of Fis1, promoting mitochondrial fission and exacerbating cellular apoptosis.

There was a mistake in the caption of Figure 5 as published. Instead of “Pathogenesis associated with Ubiquitination and sepsis-induced acute kidney injury” it should be “Pathogenesis associated with lactylation and sepsis-induced acute kidney injury”. The corrected caption of Figure 5 appears below.

The original article has been updated.

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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: acute kidney injury, sepsis, post-translational modifications, sepsis-induced acute, kidney injury, inflammation

Citation: Song L, Jiang W, Liu K, Wang J, Gong W, Yu J and Zheng R (2025) Correction: Post-translational modifications in sepsis-induced acute kidney injury: mechanisms and perspectives. Front. Pharmacol. 16:1710281. doi: 10.3389/fphar.2025.1710281

Received: 22 September 2025; Accepted: 25 September 2025;
Published: 10 October 2025.

Edited and reviewed by:

Edgar Jaimes, Memorial Sloan Kettering Cancer Center, United States

Copyright © 2025 Song, Jiang, Liu, Wang, Gong, Yu and Zheng. 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: Jiangquan Yu, eXVqaWFuZ3F1YW4yMDIxQDE2My5jb20=; Ruiqiang Zheng, emhlbmdydWlxaWFuZzIwMjFAMTYzLmNvbQ==

†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.