Evidence map›Paper›PMID 42908978›Full record

ArticleFrontiers in immunology2026

tACS suppresses M1 polarization of microglia after spinal cord injury through the cGMP-PKG signaling pathway.

Haidi Bi, Ke Huang, Xiaojun Zhou

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Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Haidi BiSchool of Public Health, Jiangxi Medical College, Nanchang University, Nanchang, China.
Ke HuangSchool of Public Health, Jiangxi Medical College, Nanchang University, Nanchang, China.
Xiaojun ZhouSchool of Public Health, Jiangxi Medical College, Nanchang University, Nanchang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Strategies for repairing spinal cord injury (SCI) emphasize blocking the shift of microglia to the pro-inflammatory M1 phenotype, lowering neuroinflammation, and fostering neuronal survival. The cGMP-PKG pathway modulates immune cell function by decreasing the secretion of pro-inflammatory elements such as IL-1β and TNF and boosting the levels of the anti-inflammatory element IL-10, thereby alleviating inflammatory responses. Additionally, transcranial alternating current stimulation (tACS) at specific frequencies may indirectly regulate immune cell activity and inflammatory cytokine secretion by modulating the autonomic nervous system, thereby demonstrating anti-inflammatory potential. Objective: To assess how tACS influences microglial polarization following SCI and investigate the underlying molecular mechanisms. Methods: Proteomics sequencing, Western blotting, ELISA, Nissl staining, hematoxylin and eosin (HE) staining, real-time quantitative PCR (qPCR), immunofluorescence, live/dead staining and other experimental techniques were employed. Furthermore, an Results: The polarization of glial cells towards the M1 proinflammatory phenotype was partially suppressed by tACS, thereby alleviating neuroinflammation and improving neuronal survival to promote functional recovery after SCI. Mechanistic studies revealed that tACS modulates the conversion of the glial inflammatory phenotype by initiating the cGMP-PKG signaling pathway, thereby offering neuroprotective and anti-inflammatory effects. Conclusion: The activity of the cGMP-PKG signaling pathway is upregulated by tACS, thereby modulating microglial polarization, suppressing neuroinflammation and protecting neurons from inflammatory injury. As a non-invasive neuromodulation technique, tACS holds potential as a therapeutic approach for SCI.

Indexed as

Cyclic GMPCyclic GMP-Dependent Protein KinasesMicrogliaSignal TransductionSpinal Cord InjuriesAnimalsCytokinesDisease Models, AnimalFemaleRatsRats, Sprague-DawleyRecovery of FunctionCyclic GMPCyclic GMP-Dependent Protein KinasesCytokinescGMP-PKGmicroglial polarizationneuroinflammationspinal cord injury repairTACs

Identifiers

PMID42908978
PMCPMC13683643

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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.