1Department of Emergency Medicine, the First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China
2Soochow University Campus Hospital, Soochow University, Suzhou, Jiangsu, China
3Department of Emergency Medicine, the First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China
*Corresponding author: Feng Xu, Department of Emergency Medicine, the First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China. Email address: [email protected]
Received 11 March 2026; Accepted 11 March 2026; Available online 24 March 2026
Copyright: Bu Z, et al.
License: This open access article is licensed under Creative Commons Attribution 4.0 International (CC BY 4.0). http://creativecommons.org/licenses/by/4.0/
In the abovementioned article, the authors wish to correct several references that were unrelated to the subject of the article and/or inappropriate for the context in which they were cited. These corrections concern citation accuracy only and do not affect the experimental data, results, or the conclusions of the study.
In the Introduction, the sentence stating that the central nervous system, especially the brain, is profoundly affected in sepsis was incorrectly supported by Reference 1. In addition, the statement that mitochondrial dysfunction is intrinsically linked to neurological deficits and the progression of sepsis-associated encephalopathy was incorrectly linked to Reference 4, and the sentence stating that mitochondrial perturbation can dramatically affect cerebral tissue was incorrectly linked in part to Reference 6. These citations have been corrected to literature directly related to sepsis-associated encephalopathy and sepsis-induced brain mitochondrial dysfunction, and the surrounding numbering has been revised accordingly.
In the Introduction, the statement that sirtuin 1 has protective relevance in sepsis-associated encephalopathy was incorrectly linked to Reference 9. This citation has been corrected to a study directly supporting the involvement of the NAD+/SIRT1 pathway in sepsis-associated encephalopathy.
In the Discussion, the sentence interpreting the safe concentration range of cimifugin for subsequent experiments was unnecessarily linked to Reference 13, which was unrelated to the specific context. Because this statement was based on the authors’ own findings, the citation has been removed.
In the Discussion, the sentence stating that SIRT1 and Nrf2 are key regulators in cellular stress response and play important roles in antioxidant, anti-inflammatory, and anti-apoptotic responses was incorrectly linked to References 19 and 20. These citations have been corrected to appropriate literature sources addressing the roles of SIRT1 and Nrf2 in inflammation, oxidative stress, and cellular protection.
The reference list and in-text citation numbering have been updated accordingly. The authors apologize for these errors and any confusion they may have caused.
Reference List 1: Replace Reference 1 after the sentence: “The central nervous system—specifically the brain—is profoundly affected.”
Reference List 2: Replace Reference 4 after the sentence: “Current evidence indicates that mitochondrial dysfunction, leading to energy metabolism aberrations and unchecked radical accumulation, is intrinsically linked to the onset of neurological deficits and the progression to SAE in septic patients.”
Reference List 3: Replace Reference 6 in the sentence: “Given the brain’s substantial energy and oxygen requisites, any mitochondrial perturbation can dramatically affect cerebral tissue, precipitating a cascade of anomalous neurological outcomes.”
Reference List 4: Replace Reference 9 after the sentence: “Concurrently, the sirtuins (SIRT) protein ensemble, with a spotlight on its isoform sirtuin 1, has emerged as a crucial mediator in energy metabolism, exhibiting protective attributes against sepsis-associated encephalopathy.”
Remove Reference 13 from the sentence discussing the safe concentration range in the Discussion.
Reference List 5: Replace References 19 and 20 after the sentence: “SIRT1 and Nrf2 are key regulators in cellular stress response and play important roles in cellular anti-oxidant, anti-inflammatory, and antiapoptotic responses.”
The authors declare that no AI-assisted tools were used in the preparation of this manuscript. All references should be manually verified for accuracy and relevance before final submission.
1. Mazeraud A, Righy C, Bouchereau E, Benghanem S, Bozza FA, Sharshar T. Septic-associated encephalopathy: A comprehensive review. Neurotherapeutics. 2020;17(2):392–403. 10.1007/s13311-020-00862-1
2. d’Avila JCP, Santiago AP, Amâncio RT, Galina A, Oliveira MF, Bozza FA. Sepsis induces brain mitochondrial dysfunction. Crit Care Med. 2008;36(6):1925–32. 10.1097/CCM.0b013e3181760c4b
3. Li H, Liu Q, Zhu CL, Sun XY, Sun CY, Yu CM, et al. β-Nicotinamide mononucleotide activates NAD+/SIRT1 pathway and attenuates inflammatory and oxidative responses in the hippocampus regions of septic mice. Redox Biol. 2023;63:102745. 10.1016/j.redox.2023.102745
4. Yang Y, Liu Y, Wang Y, Chao Y, Zhang J, Jia Y, et al. Regulation of SIRT1 and its roles in inflammation. Front Immunol. 2022;13:831168. 10.3389/fimmu.2022.831168
5. Saha S, Buttari B, Panieri E, Profumo E, Saso L. An overview of Nrf2 signaling pathway and its role in inflammation. Molecules. 2020;25(22):5474. 10.3390/molecules25225474