Evidence map›Paper›PMID 40457153›Full record

ArticleNeurocritical care2026

Hypothermia Alleviates TBI-Induced Tau Hyperphosphorylation Through RBM3-Dependent GSK-3β and AMPK Pathways.

Bingjin Liu, Qunfang Zhao, Qingqing Shi, Weiqi Xu, Fangxiao Shi, Ruhui Yang, Xinwen Zhou

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Article in Neurocritical care, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

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0cells of the map it votes in
4citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Post-Translational Modifications in Traumatic Brain Injury: Decoding the Proteomic Landscape and Molecular Mechanisms of Secondary Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Bingjin LiuNew Dosage Form and Pharmacology Research Institute, School of Medicine and Pharmaceutical Engineering, Taizhou Vocational and Technical College, Taizhou, China.
Qunfang ZhaoTaizhou Vocational and Technical College, Taizhou, China.
Qingqing ShiDepartment of Anesthesiology, Taizhou Municipal Hospital, Taizhou, China.
Weiqi XuKey Laboratory of Neurological Diseases of Education Ministry, Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Fangxiao ShiKey Laboratory of Neurological Diseases of Education Ministry, Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Ruhui YangNew Dosage Form and Pharmacology Research Institute, School of Medicine and Pharmaceutical Engineering, Taizhou Vocational and Technical College, Taizhou, China.
Xinwen ZhouKey Laboratory of Neurological Diseases of Education Ministry, Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. zhouxinwen@hust.edu.cn.ORCID 0009-0008-6675-2199

Funding

National Natural Science Foundation of China 81671262Natural Science Foundation of Zhejiang Province LTGY23H090002
6 · The paper itself

Abstract

backgroundTraumatic brain injury (TBI) often results in tau hyperphosphorylation, a key pathological feature of neurodegenerative diseases such as Alzheimer's disease. Hypothermia (HT) is a promising therapeutic intervention for TBI, but the underlying molecular mechanisms remain unclear. This study investigates the role of RNA-binding motif protein 3 (RBM3) in mediating the neuroprotective effects of HT on tau phosphorylation and its involvement in glycogen synthase kinase 3 beta (GSK-3β) and AMP-activated protein kinase (AMPK) signaling.

methodsWe used a TBI mouse model to assess the effects of HT on tau phosphorylation using Western blotting and immunohistochemistry. The phosphorylation status of GSK-3β (Ser9) and AMPK (Thr172) was also analyzed to explore key signaling pathways. RBM3 expression was modulated using RBM3 short hairpin RNA (knockdown) and adenovirus-RBM3 plasmid (overexpression) to determine its role in HT-induced changes in tau phosphorylation.

resultsHypothermia treatment significantly reduced tau hyperphosphorylation in TBI mice compared with controls. Western blotting revealed a significant increase in GSK-3β Ser9 phosphorylation (p < 0.01) and AMPK Thr172 phosphorylation (p < 0.05) in the HT group. Manipulation of RBM3 expression showed that both RBM3 knockdown and overexpression affected the extent of tau dephosphorylation mediated by HT. Specifically, RBM3 overexpression enhanced the protective effects of HT, whereas knockdown diminished its efficacy.

conclusionsOur findings suggest that RBM3 is a crucial mediator of the neuroprotective effects of hypothermia in TBI, acting through modulation of GSK-3β and AMPK signaling pathways. These results provide new insights into the molecular mechanisms of TBI treatment and highlight RBM3 as a potential therapeutic target for neurodegenerative diseases associated with tauopathies. Limitations include the need for further validation in clinical models.

Indexed as

AMP-Activated Protein KinasesBrain Injuries, TraumaticGlycogen Synthase Kinase 3 betaHypothermia, InducedRNA-Binding Proteinstau ProteinsAnimalsDisease Models, AnimalMaleMiceMice, Inbred C57BLPhosphorylationSignal TransductionAMP-Activated Protein KinasesGlycogen Synthase Kinase 3 betaRbm3 protein, mouseRNA-Binding Proteinstau ProteinsAMP-activated protein kinaseGlycogen synthase kinase-3βHypothermiaRNA-binding motif protein 3Tau phosphorylationTraumatic brain injury

Identifiers

PMID40457153

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.