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Abstract:
Retraction: "Effect of microRNA-186 on oxidative stress injury of neuron by targeting interleukin 2 through the janus kinase-signal transducer and activator of transcription pathway in a rat model of Alzheimer's disease," by Dong-Mei Wu, Xin Wen, Yong-Jian Wang, Xin-Rui Han, Shan Wang, Min Shen, Shao-Hua Fan, Juan Zhuang, Zi-Feng Zhang, Qun Shan, Meng-Qiu Li, Bin Hu, Chun-Hui Sun, Jun Lu, Gui-Quan Chen, Yuan-Lin Zheng, J Cell Physiol. 2018; 9488-9502: The above article, published online on 11 July 2018 in Wiley Online Library (https://onlinelibrary.wiley.com/doi/10.1002/jcp.26843) has been retracted by agreement between the journal's Editor in Chief, Prof. Dr. Gregg Fields, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. A detailed investigation revealed that several image elements of the experimental data were published elsewhere in a different scientific context. Thus, the editors consider the conclusions of this article to be invalid.
Insights
This study on Alzheimer's disease is retracted due to data irregularities. The article investigated microRNA-186's effect on neuronal oxidative stress, but image data was found duplicated in other contexts, invalidating the findings.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Context:
- Alzheimer's disease (AD) is a neurodegenerative disorder characterized by oxidative stress and neuronal injury.
- MicroRNAs (miRNAs) play crucial roles in regulating gene expression and cellular processes relevant to AD pathogenesis.
- The Janus Kinase-Signal Transducer and Activator of Transcription (JAK-STAT) pathway is implicated in neuroinflammation and neuronal survival.
Purpose:
- To investigate the effect of microRNA-186 (miR-186) on oxidative stress injury in neurons.
- To explore the potential mechanism involving the targeting of Interleukin-2 (IL-2) via the JAK-STAT pathway.
- To evaluate these effects in a rat model of Alzheimer's disease.
Summary:
- The retracted article proposed that microRNA-186 modulates neuronal oxidative stress in an Alzheimer's disease rat model.
- It suggested a mechanism where miR-186 targets Interleukin-2, thereby influencing the JAK-STAT signaling pathway.
- The study aimed to elucidate the role of this specific miRNA in the context of AD-related neuronal damage.
Impact:
- The findings, if valid, could have offered insights into novel therapeutic targets for Alzheimer's disease by modulating miRNA and cytokine signaling.
- Understanding the interplay between miR-186, IL-2, and the JAK-STAT pathway could inform future research directions in neuroprotection.
- However, the retraction due to duplicated image data invalidates these potential implications and necessitates caution in citing this work.
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