RETRACTED: Tangzhiqing-mediated NRF2 reduces autophagy-dependent ferroptosis to mitigate diabetes-related cognitive impairment neuronal damage.

IF 2.2 4区 医学 Q3 GERIATRICS & GERONTOLOGY
Lingyan Qiu, Kai Chen, Xu Wang, Yun Zhao
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引用次数: 0

Abstract

The publisher of Rejuvenation Research officially retracts the article entitled, "Tangzhiqing-mediated NRF2 reduces autophagy-dependent ferroptosis to mitigate diabetes-related cognitive impairment neuronal damage," by Lingyan Qiu, Mr. Kai Chen, Prof. Xu Wang, and Ms. Yun Zhao. (Rejuvenation Res 2023; epub 6 Jun; doi: 10.1089/rej.2023.0013). After the acceptance and Instant Online publication of the paper, the authors were contacted repeatedly regarding their page proofs, and for further clarification of unresolved issues within the paper. All attempts to reach the authors were unsuccessful. Concurrently, the publisher identified a problematic overlap with a paper published in 2023 in Endocrine, Metabolic & Immune Disorders - Drug Targets.1 This paper was subsequently withdrawn. These troubling details have led the editorial leadership of Rejuvenation Research to lose confidence in the validity of the submission and to retract the paper. All authors were notified of the decision to retract the paper via email. The lead author, Lingyan Qiu, and the corresponding author, Xu Wang, quickly responded and appealed the decision to retract. The appeal was denied. Reference 1. https://www.eurekaselect.com/article/132631. Withdrawn: Experimental study on NRF2 mediated by Chinese medicine tangzhiqing to reduce autophagy-dependent ferroptosis and alleviate neuron damage in HT22 mice with diabetes-related cognitive disorder. 22 June, 2023; DOI: 10.2174/1871530323666230622151649 Diabetes is a chronic condition defined by the body's inability to process glucose. The most common form, diabetes mellitus, reflects the body's insulin resistance, which leads to long-term raised glucose blood levels. These levels can cause oxidative damage, cell stress, and excessive autophagy throughout the body, including the nervous system. Diabetes-related cognitive impairment (DCI) results from chronic elevation of blood glucose, and as diabetes cases continue to rise, so too do comorbidities such as DCI. Although there are medications to address high blood glucose, there are few that can inhibit excessive autophagy and cell death. Therefore, we investigated if the Traditional Chinese Medicine, Tangzhiqing (TZQ), can reduce the impact of DCI in a high-glucose cell model. We used commercially available kits to evaluate cell viability, mitochondrial activity, and oxidative stress. We found that TZQ treatment increased cell viability, ensured continued mitochondrial activity, and reduced reactive oxygen species. We also found that TZQ functions by increasing NRF2 activity, which decreases the ferroptotic-associated pathways that involve p62, HO-1, and GPX4. Therefore, TZQ should be further investigated for its role in reducing DCI.

抑制:唐志清介导的NRF2减少自噬依赖性脱铁症,减轻糖尿病相关的认知障碍神经元损伤。
《再生研究》的出版商正式撤回了邱凌燕、陈凯先生、王旭教授和赵女士的文章,题为“糖治清介导的NRF2减少自噬依赖性铁蛋白脱失,减轻糖尿病相关的认知障碍神经元损伤”。(Rejuvenation Res 2023;epub 6 Jun;doi:10.1089/rej.2023.0013)。在论文被接受并即时在线发表后,多次联系作者,询问他们的页面校样,并进一步澄清论文中未解决的问题。所有联系作者的尝试都没有成功。与此同时,出版商发现与2023年发表在《内分泌、代谢和免疫疾病-药物靶点》上的一篇论文存在问题重叠。1这篇论文随后被撤回。这些令人不安的细节导致《复兴研究》的编辑领导层对提交的论文的有效性失去了信心,并撤回了论文。所有作者都收到了通过电子邮件撤回论文的决定通知。主要作者邱凌燕和通讯作者徐旺迅速做出回应,并对撤回决定提出上诉。上诉被驳回。参考文献1。https://www.eurekaselect.com/article/132631.退出:中药唐志清介导的NRF2减少糖尿病相关认知障碍HT22小鼠自噬依赖性脱铁和减轻神经元损伤的实验研究。2023年6月22日;DOI:10.2174/18715530323666230622151649糖尿病是一种由身体无法处理葡萄糖定义的慢性疾病。最常见的形式是糖尿病,它反映了身体的胰岛素抵抗,从而导致血糖水平长期升高。这些水平会导致氧化损伤、细胞应激和全身过度自噬,包括神经系统。糖尿病相关认知障碍(DCI)是由慢性血糖升高引起的,随着糖尿病病例的持续增加,DCI等合并症也在增加。尽管有治疗高血糖的药物,但很少有能抑制过度自噬和细胞死亡的药物。因此,我们研究了中药汤之清(TZQ)是否可以在高糖细胞模型中减少DCI的影响。我们使用市售试剂盒来评估细胞活力、线粒体活性和氧化应激。我们发现TZQ处理增加了细胞活力,确保了线粒体的持续活性,并减少了活性氧。我们还发现TZQ通过增加NRF2活性发挥作用,从而降低涉及p62、HO-1和GPX4的脱铁相关途径。因此,TZQ在降低DCI方面的作用需要进一步研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Rejuvenation research
Rejuvenation research 医学-老年医学
CiteScore
4.50
自引率
0.00%
发文量
41
审稿时长
3 months
期刊介绍: Rejuvenation Research publishes cutting-edge, peer-reviewed research on rejuvenation therapies in the laboratory and the clinic. The Journal focuses on key explorations and advances that may ultimately contribute to slowing or reversing the aging process, and covers topics such as cardiovascular aging, DNA damage and repair, cloning, and cell immortalization and senescence. Rejuvenation Research coverage includes: Cell immortalization and senescence Pluripotent stem cells DNA damage/repair Gene targeting, gene therapy, and genomics Growth factors and nutrient supply/sensing Immunosenescence Comparative biology of aging Tissue engineering Late-life pathologies (cardiovascular, neurodegenerative and others) Public policy and social context.
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