Evidence map›Paper›PMID 40624993›Full record

ArticleNeurospine2025

Transcranial Optogenetic Stimulation Promotes Corticospinal Tract Axon Regeneration to Repair Spinal Cord Injury by Activating the JAK2/STAT3 Pathway.

Yuan-Huan Ma, Hong-Ying Chen, Qing-Shuai Wei, Li-Zhi Peng, Ke-Jun Zhang, Qing-Wen Deng, Lai-Jian Wang, Zhou Liu, Bi-Qin Lai, Ying Ding and 5 more

Abstract read
In one paragraph

Article in Neurospine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Yuan-Huan MaKey Laboratory for Stem Cells and Tissue Engineering, Sun Yat-sen University, Ministry of Education, Guangzhou, China.
Hong-Ying ChenDepartment of Rehabilitation Medicine, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Qing-Shuai WeiKey Laboratory for Stem Cells and Tissue Engineering, Sun Yat-sen University, Ministry of Education, Guangzhou, China.
Li-Zhi PengDepartment of Histology and Embryology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Ke-Jun ZhangLab of Stem Cell Biology and Innovative Research of Chinese Medicine; National Institute of Stem Cell Clinical Research, Guangdong Provincial Hospital of Chinese Medicine/Guangdong Academy of Chinese Medicine/The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.
Qing-Wen DengKey Laboratory for Stem Cells and Tissue Engineering, Sun Yat-sen University, Ministry of Education, Guangzhou, China.
Lai-Jian WangGuangdong Provincial Key Laboratory of Brain Function and Disease, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Zhou LiuGuangdong Key Laboratory of Age-Related Cardiocerebral Diseases, Institute of Neurology, Guangdong Medical University, Zhanjiang, China.
Bi-Qin LaiKey Laboratory for Stem Cells and Tissue Engineering, Sun Yat-sen University, Ministry of Education, Guangzhou, China.
Ying DingKey Laboratory for Stem Cells and Tissue Engineering, Sun Yat-sen University, Ministry of Education, Guangzhou, China.
Ge LiKey Laboratory for Stem Cells and Tissue Engineering, Sun Yat-sen University, Ministry of Education, Guangzhou, China.
Bin JiangGuangdong Provincial Key Laboratory of Brain Function and Disease, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Yue LanDepartment of Rehabilitation Medicine, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Xiang ZengLab of Stem Cell Biology and Innovative Research of Chinese Medicine; National Institute of Stem Cell Clinical Research, Guangdong Provincial Hospital of Chinese Medicine/Guangdong Academy of Chinese Medicine/The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.
Yuan-Shan ZengKey Laboratory for Stem Cells and Tissue Engineering, Sun Yat-sen University, Ministry of Education, Guangzhou, China.

Funding

Guangzhou Basic and Applied Basic Research Foundation 2023A03J0626Guangzhou First People's Hospital KYQD20210017Guangzhou Municipal Science and Technology Program 202206010197Guangzhou Municipal Science and Technology Program 2025A04J4286National Natural Science Foundation of China 31900975National Natural Science Foundation of China 81891002National Natural Science Foundation of China 818981003National Natural Science Foundation of China 81974357Natural Science Foundation of Guangdong 2023A1515030254Natural Science Foundation of Guangdong 2024A1515220057Startup Grant of Guangdong Hospital of Chinese Medicine 2022KT1032
6 · The paper itself

Abstract

objectiveRegeneration of corticospinal tract (CST) axons after spinal cord injury (SCI) is a key element in rebuilding neuronal connections to restore voluntary motor function. However, it remains challenging owing to limited effective interventions. This study adopted a modified transcranial optogenetic technique to stimulate CST axon regeneration into the injury site of completely transected SCI and explore the underlying molecular mechanisms.

methodsA novel optogenetic light emitting diode (LED) device was used to stimulate the brain motor cortex in channelrhodopsin-2-yellow fluorescent protein (ChR2-YFP) transgenic mice to observe the regeneration of CST axons in the injury site of a complete SCI. The LED device was also used In vitro to stimulate the motor cortex slices of the transgenic mouse brain for observing the outgrowth of their neurites.

resultsAfter transcranial optogenetic stimulation, the pyramidal neurons of bilateral cerebral motor cortices, in ChR2-YFP transgenic mice were activated, CST axons regenerated into the injury site of the spinal cord, and the motor function of the paralyzed hindlimbs improved. Proteomic analysis revealed that CST axon regeneration was associated with the activation of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway in the cerebral motor cortices. In vitro LED blue light illumination enhanced the outgrowth of neurites from the brain slices of transgenic mice. Treatment with a JAK2/STAT3 inhibitor led to a significant attenuation of neurite outgrowth.

conclusionThe modified transcranial optogenetic technique stimulated bilateral motor cortices, in the brains of ChR2-YFP transgenic mice. It increased the excitability of pyramidal neurons in the motor cortices, and promoted CST axon regeneration by activating the JAK2/STAT3 pathway, repairing complete SCI.

Indexed as

Axonal regenerationComplete spinal cord injuryJAK2/STAT3 pathwayOptogenetic LED deviceProteomics analysisTranscranial optogenetics

Identifiers

PMID40624993
PMCPMC12242751

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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.