Evidence map›Paper›PMID 22263913›Full record

ArticleNanotoxicology2013

Reactive oxygen species-mediated p38 MAPK regulates carbon nanotube-induced fibrogenic and angiogenic responses.

Neelam Azad, Anand Krishnan V Iyer, Liying Wang, Yuxin Liu, Yongju Lu, Yon Rojanasakul

Abstract read
In one paragraph

Article in Nanotoxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 90 citations in OpenAlex.

  1. Review
  2. RSC advances · 2022
    Review
  3. Review
  4. Review
  5. Review
  6. Developmental toxicity of carbon nanoparticles during embryogenesis in chicken.Environmental science and pollution research international · 2020
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Nitrolipids in kidney physiology and disease.Nitric oxide : biology and chemistry · 2018
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Silica nanoparticles induce liver fibrosis via TGF-βInternational journal of nanomedicine · 2017
    Article
  18. Review
  19. Article
  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

6 authors at 3 institutions in 1 country.

Neelam AzadDepartment of Pharmaceutical Sciences, Hampton University, Hampton, VA 23668, USA.
Anand Krishnan V Iyer
Liying Wang
Yuxin Liu
Yongju Lu
Yon Rojanasakul
West Virginia University · USHampton University · USNational Institute for Occupational Safety and Health · US

Funding

Prediction and Mechanism of Carbon Nanotube-Induced FibrosisR01HL095579 · NHLBI · WEST VIRGINIA UNIVERSITY · PI ROJANASAKUL, YON · 2010 to 2013
$1.5M
Impact of Oxidative Stress-Regulated Angiogenesis in Pulmonary FibrosisSC1HL112630 · NHLBI · HAMPTON UNIVERSITY · PI AZAD, NEELAM · 2011 to 2015
$1.3M
NHLBI NIH HHS R01 HL095579NHLBI NIH HHS R01-HL095579NHLBI NIH HHS SC1 HL112630
6 · The paper itself

Abstract

Single-walled carbon nanotubes (SWCNTs) are fibrous nanoparticles that are being used widely for various applications including drug delivery. SWCNTs are currently under special attention for possible cytotoxicity. Recent reports suggest that exposure to nanoparticles leads to pulmonary fibrosis. We report that SWCNT-mediated interplay of fibrogenic and angiogenic regulators leads to increased angiogenesis, which is a novel finding that furthers the understanding of SWCNT-induced cytotoxicity. SWCNTs induce fibrogenesis through reactive oxygen species-regulated phosphorylation of p38 mitogen-activated protein kinase (MAPK). Activation of p38 MAPK by SWCNTs led to the induction of transforming growth factor (TGF)-β1 as well as vascular endothelial growth factor (VEGF). Both TGF-β1 and VEGF contributed significantly to the fibroproliferative and collagen-inducing effects of SWCNTs. Interestingly, a positive feedback loop was observed between TGF-β1 and VEGF. This interplay of fibrogenic and angiogenic mediators led to increased angiogenesis in response to SWCNTs. Overall this study reveals key signalling molecules involved in SWCNT-induced fibrogenesis and angiogenesis.

Indexed as

Neovascularization, PathologicCell LineCell ProliferationCollagenDose-Response Relationship, DrugEndothelial CellsEnzyme ActivationFeedback, PhysiologicalFibroblastsFibrosisHumansNanotubes, CarbonOxidative Stressp38 Mitogen-Activated Protein KinasesPulmonary FibrosisReactive Oxygen SpeciesCollagenNanotubes, Carbonp38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesTGFB1 protein, humanTransforming Growth Factor beta1Vascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID22263913
PMCPMC4089498
OpenAlexW2123299551

What OpenQuestion holds

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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.