Evidence map›Paper›PMID 36933884›Full record

ArticleJournal of advanced research2024

Polystyrenenanoplastics lead to ferroptosis in the lungs.

Yuhao Wu, Junke Wang, Tianxin Zhao, Mang Sun, Maozhu Xu, Siyi Che, Zhengxia Pan, Chun Wu, Lianju Shen

Open access · goldAbstract read
In one paragraph

Article in Journal of advanced research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 95 citations in OpenAlex.

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  17. Forever particles: histochemistry in the plasticene age.European journal of histochemistry : EJH · 2025
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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

9 authors at 5 institutions in 1 country.

Yuhao WuDepartment of Cardiothoracic Surgery, Children's Hospital of Chongqing Medical University, Chongqing, China; Pediatric Research Institute, Chongqing Key Laboratory of Pediatrics, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, Children's Hospital of Chongqing Medical University, China.
Junke WangThe Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Tianxin ZhaoDepartment of Pediatric Surgery, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, China.
Mang SunThe Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Maozhu XuPediatric Research Institute, Chongqing Key Laboratory of Pediatrics, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, Children's Hospital of Chongqing Medical University, China; Department of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Chongqing, China.
Siyi ChePediatric Research Institute, Chongqing Key Laboratory of Pediatrics, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, Children's Hospital of Chongqing Medical University, China; Department of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Chongqing, China.
Zhengxia PanDepartment of Cardiothoracic Surgery, Children's Hospital of Chongqing Medical University, Chongqing, China; Pediatric Research Institute, Chongqing Key Laboratory of Pediatrics, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, Children's Hospital of Chongqing Medical University, China.
Chun WuDepartment of Cardiothoracic Surgery, Children's Hospital of Chongqing Medical University, Chongqing, China; Pediatric Research Institute, Chongqing Key Laboratory of Pediatrics, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, Children's Hospital of Chongqing Medical University, China.
Lianju ShenPediatric Research Institute, Chongqing Key Laboratory of Pediatrics, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, Children's Hospital of Chongqing Medical University, China. Electronic address: 482061@hospital.cqmu.edu.cn.
Children's Hospital of Chongqing Medical University · CNChongqing Medical University · CNDalian Medical University · CNGuangzhou Medical University · CNSecond Affiliated Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionIt has been shown that polystyrenenanoplastic (PS-NP) exposure induces toxicity in the lungs.

objectivesThis study aims to provide foundational evidence to corroborate that ferroptosis and abnormal HIF-1α activity are the main factors contributing to pulmonary dysfunction induced by PS-NP exposure.

methodsFifty male and female C57BL/6 mice were exposed to distilled water or 100 nm or 200 nm PS-NPs via intratracheal instillation for 7 consecutive days. Hematoxylin and eosin (H&E) and Masson trichrome staining were performed to observe the histomorphological changes in the lungs. To clarify the mechanisms of PS-NP-induced lung injury, we used 100 μg/ml, 200 μg/ml and 400 μg/ml 100 or 200 nm PS-NPs to treat the human lung bronchial epithelial cell line BEAS-2B for 24 h. RNA sequencing (RNA-seq) of BEAS-2B cells was performed following exposure. The levels of glutathione, malondialdehyde, ferrous iron (Fe

resultsH&E staining revealed substantial perivascular lymphocytic inflammation in a bronchiolocentric pattern, and Masson trichrome staining demonstrated critical collagen deposits in the lungs after PS-NP exposure. RNA-seq revealed that the differentially expressed genes in PS-NP-exposed BEAS-2B cells were enriched in lipid metabolism and iron ion binding processes. After PS-NP exposure, the levels of malondialdehyde, Fe

conclusionPS-NP exposure caused ferroptosis in bronchial epithelial cells by activating the HIF-1α/HO-1 signaling pathway, and eventually led to lung injury.

Indexed as

FerroptosisLung InjuryAnimalsBronchiEosine Yellowish-(YS)FemaleGlutathioneHumansIronMaleMalondialdehydeMiceMice, Inbred C57BLReactive Oxygen SpeciesEosine Yellowish-(YS)GlutathioneIronMalondialdehydeReactive Oxygen SpeciesBronchial epithelial cellsFerroptosisLung injuryPolystyrene nanoplastics

Identifiers

PMID36933884
PMCPMC10834790
OpenAlexW4327559999

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.