Evidence map›Paper›PMID 41367063›Full record

ArticleAnimal models and experimental medicine2025

STING deficiency promotes motor recovery in mice following brachial plexus root avulsion.

Yu Peng, Ying Zhang, Shenhui Yang, Lu He, Shuangxi Chen

Abstract read
In one paragraph

Article in Animal models and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

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0cells of the map it votes in
3citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Yu PengDepartment of Neurology, Multi-Omics Research Center for Brain Disorders, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Ying ZhangInstitute of Pharmacy and Pharmacology, Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, Hunan, China.
Shenhui YangDepartment of Neurosurgery, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Lu HeDepartment of Neurosurgery, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Shuangxi ChenDepartment of Neurology, Multi-Omics Research Center for Brain Disorders, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.ORCID 0000-0001-7711-9171

Funding

Health Research Project of Hunan Provincial Health Commission W20243271National Natural Science Foundation of China 82301581Natural Science Foundation of Hunan Province 2024JJ6401
6 · The paper itself

Abstract

backgroundBrachial plexus root avulsion (BPRA), a well-known form of peripheral nerve injury, results in motor function loss in the affected forelimb due to motoneuron (MN) death, which may be influenced by neuroinflammation following a lesion in the spinal cord. Although synthase-stimulator of interferon genes (STING) signaling can contribute to chronic inflammation and tissue damage in a number of pathological conditions, the essential role of STING signaling in BPRA remains to be reported. Based on our previous findings that the STING mRNA level is upregulated in the anterior horn of the segment of the affected spinal cords of mice with BPRA, STING may be associated with motor recovery in BPRA.

methodsIn the present study, STING knockout transgenic mice were used to establish a BPRA re-implantation model, which was followed by behavioral tests, histochemical staining and quantitative reverse transcription polymerase chain reaction.

resultsThe results demonstrated that STING deficiency can increase the body weight, promote motor recovery, decrease MN death, inhibit pyroptosis and neuroinflammation, increase remyelination, and reduce the atrophy of the biceps brachii in mice with BPRA.

conclusionThese combined results suggest that inhibition of STING may be a promising strategy for treating BPRA.

Indexed as

Brachial PlexusMembrane ProteinsRadiculopathyRecovery of FunctionAnimalsDisease Models, AnimalMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMotor NeuronsSTING ProteinMembrane ProteinsSting1 protein, mouseSTING Proteinbrachial plexus root avulsion (BPRA)motoneuron (MN)neuroinflammationsynthase‐stimulator of interferon genes (STING)

Identifiers

PMID41367063
PMCPMC12884437

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