Evidence map›Paper›PMID 28194639›Full record

ArticleCardiovascular toxicology2017

Ultrafine Particulate Matter Increases Cardiac Ischemia/Reperfusion Injury via Mitochondrial Permeability Transition Pore.

Nathan A Holland, Chad R Fraiser, Ruben C Sloan, Robert B Devlin, David A Brown, Christopher J Wingard

Open access · greenAbstract read
In one paragraph

Article in Cardiovascular toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
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  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Characterization of ambient PMEnvironmental geochemistry and health · 2021
    Article
  12. Cardiovascular adaptations to particle inhalation exposure: molecular mechanisms of the toxicology.American journal of physiology. Heart and circulatory physiology · 2020
    Review
  13. Trace elements and human health risks assessment of finer aerosol atmospheric particles (PMEnvironmental science and pollution research international · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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 2 institutions in 1 country.

Nathan A HollandDepartment of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
Chad R FraiserDepartment of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
Ruben C SloanDepartment of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
Robert B DevlinNational Health and Environmental Effects Research Laboratory, Environmental Public Health Division, US Environmental Protection Agency, Chapel Hill, NC, USA.
David A BrownDepartment of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
Christopher J WingardDepartment of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA. cwingard@bellarmine.edu.ORCID 0000-0002-8251-5678
East Carolina University · USEnvironmental Protection Agency · US

Funding

Synthesis and Characterization CoreU19ES019525 · NIEHS · RESEARCH TRIANGLE INSTITUTE · PI FENNELL, TIMOTHY RAYMOND · 2010 to 2014
$6.3M
Cardio-vascular Impact of Inhaled Multi-wall Carbon NanotubesR01ES016246 · NIEHS · EAST CAROLINA UNIVERSITY · PI WINGARD, CHRISTOPHER J · 2007 to 2010
$1.4M
Intramural EPA EPA999999NIEHS NIH HHS R01 ES016246NIEHS NIH HHS U19 ES019525
6 · The paper itself

Abstract

Ultrafine particulate matter (UFP) has been associated with increased cardiovascular morbidity and mortality. However, the mechanisms that drive PM-associated cardiovascular disease and dysfunction remain unclear. We examined the impact of oropharyngeal aspiration of 100 μg UFP from the Chapel Hill, NC, air shed in Sprague-Dawley rats on cardiac function, arrhythmogenesis, and cardiac ischemia/reperfusion (I/R) injury using a Langendorff working heart model. We found that exposure to UFP was capable of significantly exacerbating cardiac I/R injury without changing overall cardiac function or major changes in arrhythmogenesis. Cardiac I/R injury was attenuable with administration of cyclosporin A (CsA), suggesting a role for the mitochondrial permeability transition pore (mPTP) in UFP-associated cardiovascular toxicity. Isolated cardiac mitochondria displayed decreased Ca

Indexed as

AnimalsIsolated Heart PreparationMaleMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocardial Reperfusion InjuryParticle SizeParticulate MatterRatsRats, Sprague-DawleyMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreParticulate MatterCardiacMitochondriamPTPParticulate matterReperfusion injury

Identifiers

PMID28194639
PMCPMC5617757
OpenAlexW2588134774

What OpenQuestion holds

Textmetadata
LicenceTDM
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.