Evidence map›Paper›PMID 25395850›Full record

ArticleInternational journal of nanomedicine2014

Silica nanoparticles induce autophagy and endothelial dysfunction via the PI3K/Akt/mTOR signaling pathway.

Junchao Duan, Yongbo Yu, Yang Yu, Yang Li, Ji Wang, Weijia Geng, Lizhen Jiang, Qiuling Li, Xianqing Zhou, Zhiwei Sun

Open access · goldAbstract read
In one paragraph

Article in International journal of nanomedicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
11.2field-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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 179 citations in OpenAlex.

  1. Analyzing Molecular Determinants of Nanodrugs' Cytotoxic Effects.International journal of molecular sciences · 2025
    Pooled it
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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

10 authors at 1 institution in 1 country.

Junchao DuanSchool of Public Health, Capital Medical University, Beijing, People's Republic of China ; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, People's Republic of China.
Yongbo YuSchool of Public Health, Capital Medical University, Beijing, People's Republic of China ; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, People's Republic of China.
Yang YuSchool of Public Health, Capital Medical University, Beijing, People's Republic of China ; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, People's Republic of China.
Yang LiSchool of Public Health, Capital Medical University, Beijing, People's Republic of China ; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, People's Republic of China.
Ji WangSchool of Public Health, Capital Medical University, Beijing, People's Republic of China ; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, People's Republic of China.
Weijia GengSchool of Public Health, Capital Medical University, Beijing, People's Republic of China ; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, People's Republic of China.
Lizhen JiangSchool of Public Health, Capital Medical University, Beijing, People's Republic of China ; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, People's Republic of China.
Qiuling LiSchool of Public Health, Capital Medical University, Beijing, People's Republic of China ; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, People's Republic of China.
Xianqing ZhouSchool of Public Health, Capital Medical University, Beijing, People's Republic of China ; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, People's Republic of China.
Zhiwei SunSchool of Public Health, Capital Medical University, Beijing, People's Republic of China ; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, People's Republic of China.
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although nanoparticles have a great potential for biomedical applications, there is still a lack of a correlative safety evaluation on the cardiovascular system. This study is aimed to clarify the biological behavior and influence of silica nanoparticles (Nano-SiO2) on endothelial cell function. The results showed that the Nano-SiO2 were internalized into endothelial cells in a dose-dependent manner. Monodansylcadaverine staining, autophagic ultrastructural observation, and LC3-I/LC3-II conversion were employed to verify autophagy activation induced by Nano-SiO2, and the whole autophagic process was also observed in endothelial cells. In addition, the level of nitric oxide (NO), the activities of NO synthase (NOS) and endothelial (e)NOS were significantly decreased in a dose-dependent way, while the activity of inducible (i)NOS was markedly increased. The expression of C-reactive protein, as well as the production of proinflammatory cytokines (tumor necrosis factor α, interleukin [IL]-1β, and IL-6) were significantly elevated. Moreover, Nano-SiO2 had an inhibitory effect on the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway. Our findings demonstrated that Nano-SiO2 could disturb the NO/NOS system, induce inflammatory response, activate autophagy, and eventually lead to endothelial dysfunction via the PI3K/Akt/mTOR pathway. This indicates that exposure to Nano-SiO2 is a potential risk factor for cardiovascular diseases.

Indexed as

AutophagyCell LineEndothelial CellsHumansHuman Umbilical Vein Endothelial CellsNanoparticlesNitric OxidePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionSilicon DioxideTOR Serine-Threonine KinasesNitric OxidePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSilicon DioxideTOR Serine-Threonine Kinasesautophagyendothelial dysfunctioninflammationnitric oxidesilica nanoparticles

Identifiers

PMID25395850
PMCPMC4227623
OpenAlexW2010723293

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.