Evidence map›Paper›PMID 41817783›Full record

ArticleMolecular neurobiology2026

Silica Nanoparticles Induce BV-2 Cells Autophagy Via activation of NLRP3 inflammasome and CaMKK2 Signaling Pathways.

Tianxiang Liu, Mingqian Wang, Yuanyuan Zhang, Li Yang, Jia Zhang, Hongzhu Wei, Xinyue Li, Huan Pang, Jiali Li, Zhixuan Luo and 5 more

Abstract read
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In one paragraph

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

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Tianxiang LiuSchool of Public Health, Jilin University, Changchun, Jilin, 130021, China.
Mingqian WangSchool of Public Health, Jilin University, Changchun, Jilin, 130021, China.
Yuanyuan ZhangState Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, Changchun, 130062, China.
Li YangState Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, Changchun, 130062, China.
Jia ZhangSchool of Public Health, Jilin University, Changchun, Jilin, 130021, China.
Hongzhu WeiSchool of Public Health, Jilin University, Changchun, Jilin, 130021, China.
Xinyue LiSchool of Public Health, Jilin University, Changchun, Jilin, 130021, China.
Huan PangSchool of Public Health, Jilin University, Changchun, Jilin, 130021, China.
Jiali LiSchool of Public Health, Jilin University, Changchun, Jilin, 130021, China.
Zhixuan LuoSchool of Public Health, Jilin University, Changchun, Jilin, 130021, China.
Mengyue LiuSchool of Public Health, Jilin University, Changchun, Jilin, 130021, China.
Haiying DuSchool of Public Health, Jilin University, Changchun, Jilin, 130021, China. hydu@jlu.edu.cn.
Chao ZhaoSchool of Public Health, Jilin University, Changchun, Jilin, 130021, China. czhao0529@jlu.edu.cn.
Xiuling SongSchool of Public Health, Jilin University, Changchun, Jilin, 130021, China. songxiuling@jlu.edu.cn.
Minghua JinSchool of Public Health, Jilin University, Changchun, Jilin, 130021, China. jinmh@jlu.edu.cn.

Funding

National Natural Science Foundation of China No.81973089Natural Science Foundation of Jilin Province Science and Technology Department No.20230101137JC
6 · The paper itself

Abstract

Previous studies have shown that silica nanoparticles (SiNPs) can cause neuronal damage and neurodegenerative changes, but the specific mechanism remains incompletely understood. Using the mouse microglial BV-2 cell model, this study explored the neurotoxic mechanism of SiNPs from the perspectives of inflammation and autophagy. Results demonstrated that SiNPs exposure could reduce BV-2 cell viability, alter cell morphology, increase autophagosomes, elevate intracellular ROS levels and induce oxidative damage. It could also trigger inflammatory reactions associated with activation of the NLRP3 inflammasome. Inhibiting ROS can reduce the assembly and activation of the NLRP3 inflammasome. Furthermore, SiNPs might enhance cellular autophagy potentially via the CaMKK2/AMPKα/mTOR pathway. Inhibition of NLRP3 inflammasome could attenuate SiNPs induced inflammation and autophagy. Overall, this study confirms that SiNPs exert toxic effects on BV-2 cells, which may be associated with the excessive inflammation and autophagy they induce. SiNPs can enhance cellular autophagy via the CaMKK2/AMPKα/mTOR pathway, and the NLRP3 inflammasome plays a positive regulatory role in SiNPs induced autophagy in BV-2 cells.

Indexed as

AutophagyCalcium-Calmodulin-Dependent Protein Kinase KinaseInflammasomesNanoparticlesNLR Family, Pyrin Domain-Containing 3 ProteinSignal TransductionSilicon DioxideAMP-Activated Protein KinasesAnimalsCell LineCell SurvivalMiceMicrogliaReactive Oxygen SpeciesTOR Serine-Threonine KinasesAMP-Activated Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase KinaseCamkk2 protein, mouseInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesSilicon DioxideTOR Serine-Threonine KinasesAutophagyBV-2 cellCaMKK2-AMPKα-mTOR pathwayNLRP3 inflammasomeReactive oxygen species (ROS)Silica nanoparticles (SiNPs)

Identifiers

PMID41817783

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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.