Evidence map›Paper›PMID 24330719›Full record

ArticleParticle and fibre toxicology2013

Diesel exhaust particulate increases the size and complexity of lesions in atherosclerotic mice.

Mark R Miller, Steven G McLean, Rodger Duffin, Akeem O Lawal, Jesus A Araujo, Catherine A Shaw, Nicholas L Mills, Ken Donaldson, David E Newby, Patrick W F Hadoke

Open access · goldAbstract read
In one paragraph

Article in Particle and fibre toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
6.7field-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

56 citing papers in PubMed, 128 citations in OpenAlex.

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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 3 institutions in 2 countries.

Mark R MillerCentre for Cardiovascular Sciences, University of Edinburgh, 47 Little France Crescent, EH16 4TJ Edinburgh, Scotland, UK. mark.miller@ed.ac.uk.
Steven G McLean
Rodger Duffin
Akeem O Lawal
Jesus A Araujo
Catherine A Shaw
Nicholas L Mills
Ken Donaldson
David E Newby
Patrick W F Hadoke
University of Edinburgh · GBUniversity of California, Los Angeles · USCentre for Inflammation Research · GB

Funding

Effects of particulate air pollution on HDL function and atherosclerosisR01ES016959 · NIEHS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARAUJO, JESUS ANTONIO · 2009 to 2013
$2.4M
British Heart Foundation CH/09/002British Heart Foundation FS/10/024/28266British Heart Foundation PG/10/042/28388British Heart Foundation PG/10/42/28388British Heart Foundation PG/11/27/28842British Heart Foundation RG/10/009British Heart Foundation RG/10/9/28286Medical Research Council G0901697NIEHS NIH HHS R01 ES016959
6 · The paper itself

Abstract

objectiveDiesel exhaust particulate (DEP), a major component of urban air pollution, has been linked to atherogenesis and precipitation of myocardial infarction. We hypothesized that DEP exposure would increase and destabilise atherosclerotic lesions in apolipoprotein E deficient (ApoE-/-) mice.

methodsApoE-/- mice were fed a 'Western diet' (8 weeks) to induce 'complex' atherosclerotic plaques, with parallel experiments in normal chow fed wild-type mice. During the last 4 weeks of feeding, mice received twice weekly instillation (oropharyngeal aspiration) of 35 μL DEP (1 mg/mL, SRM-2975) or vehicle (saline). Atherosclerotic burden was assessed by en-face staining of the thoracic aorta and histological examination of the brachiocephalic artery.

resultsBrachiocephalic atherosclerotic plaques were larger in ApoE-/- mice treated with DEP (59 ± 10%) than in controls (32 ± 7%; P = 0.017). In addition, DEP-treated mice had more plaques per section of artery (2.4 ± 0.2 vs 1.8 ± 0.2; P = 0.048) and buried fibrous layers (1.2 ± 0.2 vs 0.4 ± 0.1; P = 0.028). These changes were associated with lung inflammation and increased antioxidant gene expression in the liver, but not with changes in endothelial function, plasma lipids or systemic inflammation.

conclusionsIncreased atherosclerosis is caused by the particulate component of diesel exhaust producing advanced plaques with a potentially more vulnerable phenotype. These results are consistent with the suggestion that removal of the particulate component would reduce the adverse cardiovascular effects of diesel exhaust.

Indexed as

Airway RemodelingAnimalsAorta, ThoracicApolipoproteins EBlood CoagulationBrachiocephalic TrunkC-Reactive ProteinDisease Models, AnimalFibrinogenLipidsMaleMiceMice, Inbred C57BLMice, KnockoutOropharynxOxidative StressApolipoproteins EC-Reactive ProteinFibrinogenLipidsParticulate MatterVehicle Emissions

Identifiers

PMID24330719
PMCPMC3907045
OpenAlexW2152640801

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.