Evidence map›Paper›PMID 32513195›Full record

ArticleParticle and fibre toxicology2020

Silica nanoparticles induce lung inflammation in mice via ROS/PARP/TRPM2 signaling-mediated lysosome impairment and autophagy dysfunction.

Mingxiang Wang, Jin Li, Shunni Dong, Xiaobo Cai, Aili Simaiti, Xin Yang, Xinqiang Zhu, Jianhong Luo, Lin-Hua Jiang, Binyang Du and 2 more

Open access · goldAbstract read
In one paragraph

Article in Particle and fibre toxicology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
11.8field-weighted citation impact, top 1% of its field
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

57 citing papers in PubMed, 152 citations in OpenAlex.

  1. Review
  2. Article
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  8. Pulmonary injury following exposure to amorphous silicon dioxide nanoparticles inExperimental biology and medicine (Maywood, N.J.) · 2026
    Article
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  12. Review
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  14. Review
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  17. Journal of proteome research · 2025
    Article
  18. SiOScientific reports · 2025
    Article
  19. [Advances in the development of transient receptor potential melastatin 2 channel inhibitors].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025
    Review
  20. Article
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

12 authors at 5 institutions in 3 countries.

Mingxiang WangDepartment of Toxicology, and Department of Medical Oncology of Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, P. R. China.
Jin LiDepartment of Toxicology, and Department of Medical Oncology of Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, P. R. China.
Shunni DongMOE Key Laboratory of Macromolecular Synthesis and Functionalization, Department of Polymer Science & Engineering, Zhejiang University, Hangzhou, China.
Xiaobo CaiDepartment of Toxicology, and Department of Medical Oncology of Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, P. R. China.
Aili SimaitiDepartment of Toxicology, and Department of Medical Oncology of Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, P. R. China.
Xin YangDepartment of Toxicology, and Department of Medical Oncology of Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, P. R. China.
Xinqiang ZhuDepartment of Toxicology, and Department of Medical Oncology of Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, P. R. China.
Jianhong LuoInstitute of Neuroscience, NHC and CAMS Key Laboratory of Medical Neurobiology, Zhejiang University School of Medicine, Hangzhou, P. R. China.
Lin-Hua JiangSino-UK Joint Laboratory of Brain Function and Injury and Department of Physiology and Neurobiology, Xinxiang Medical University, Xinxiang, P. R. China.
Binyang DuMOE Key Laboratory of Macromolecular Synthesis and Functionalization, Department of Polymer Science & Engineering, Zhejiang University, Hangzhou, China. duby@zju.edu.cn.
Peilin YuDepartment of Toxicology, and Department of Medical Oncology of Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, P. R. China. yupeilin@zju.edu.cn.
Wei YangDepartment of Biophysics, and Department of Neurosurgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, P. R. China. yangwei@zju.edu.cn.ORCID 0000-0003-3065-1843
Second Affiliated Hospital of Zhejiang University · CNZhejiang University · CNChemical Synthesis Lab · SGFirst Affiliated Hospital Zhejiang University · CNUniversity of Leeds · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWide applications of nanoparticles (NPs) have raised increasing concerns about safety to humans. Oxidative stress and inflammation are extensively investigated as mechanisms for NPs-induced toxicity. Autophagy and lysosomal dysfunction are emerging molecular mechanisms. Inhalation is one of the main pathways of exposing humans to NPs, which has been reported to induce severe pulmonary inflammation. However, the underlying mechanisms and, more specifically, the interplays of above-mentioned mechanisms in NPs-induced pulmonary inflammation are still largely obscure. Considered that NPs exposure in modern society is often unavoidable, it is highly desirable to develop effective strategies that could help to prevent nanomaterials-induced pulmonary inflammation.

resultsPulmonary inflammation induced by intratracheal instillation of silica nanoparticles (SiNPs) in C57BL/6 mice was prevented by PJ34, a poly (ADP-ribose) polymerase (PARP) inhibitor. In human lung bronchial epithelial (BEAS-2B) cells, exposure to SiNPs reduced cell viability, and induced ROS generation, impairment in lysosome function and autophagic flux. Inhibition of ROS generation, PARP and TRPM2 channel suppressed SiNPs-induced lysosome impairment and autophagy dysfunction and consequent inflammatory responses. Consistently, SiNPs-induced pulmonary inflammation was prevented in TRPM2 deficient mice.

conclusionThe ROS/PARP/TRPM2 signaling is critical in SiNPs-induced pulmonary inflammation, providing novel mechanistic insights into NPs-induced lung injury. Our study identifies TRPM2 channel as a new target for the development of preventive and therapeutic strategies to mitigate nanomaterials-induced lung inflammation.

Indexed as

AnimalsAutophagyInhalation ExposureLysosomesMiceMice, Inbred C57BLNanoparticlesParticle SizePneumoniaPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesSignal TransductionSilicon DioxideSurface PropertiesTRPM Cation ChannelsPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesSilicon DioxideTRPM2 protein, mouseTRPM Cation ChannelsAutophagy dysfunctionLysosomal impairmentNanoparticlesPulmonary inflammationROS/PARP/TRPM2 signaling

Identifiers

PMID32513195
PMCPMC7281956
OpenAlexW3033436779

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.