Evidence map›Paper›PMID 33948438›Full record

ArticleToxicology reports2021

Vehicle emissions-exposure alters expression of systemic and tissue-specific components of the renin-angiotensin system and promotes outcomes associated with cardiovascular disease and obesity in wild-type C57BL/6 male mice.

Benjamin L Phipps, Usa Suwannasual, JoAnn Lucero, Nicholas A Mitchell, Amie K Lund

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Toxicology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. 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

5 authors at 1 institution in 1 country.

Benjamin L PhippsAdvanced Environmental Research Institute, Department of Biological Sciences, University of North Texas, Denton, TX, 76201, USA.
Usa SuwannasualAdvanced Environmental Research Institute, Department of Biological Sciences, University of North Texas, Denton, TX, 76201, USA.
JoAnn LuceroAdvanced Environmental Research Institute, Department of Biological Sciences, University of North Texas, Denton, TX, 76201, USA.
Nicholas A MitchellAdvanced Environmental Research Institute, Department of Biological Sciences, University of North Texas, Denton, TX, 76201, USA.
Amie K LundAdvanced Environmental Research Institute, Department of Biological Sciences, University of North Texas, Denton, TX, 76201, USA.
University of North Texas · US

Funding

The Renin-Angiotensin System in Air Pollution-Mediated Exacerbation of Obesity.R15ES026795 · NIEHS · UNIVERSITY OF NORTH TEXAS · PI LUND, AMIE KATHLEEN · 2017 to 2023
$874k
MMP-9 Activity Mediates Vascular Effects of Inhaled Environmental Air PollutantsR00ES016586 · NIEHS · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI LUND, AMIE KATHLEEN · 2009 to 2011
$761k
NIEHS NIH HHS R00 ES016586NIEHS NIH HHS R15 ES026795
6 · The paper itself

Abstract

Exposure to air pollution from traffic-generated sources is known to contribute to the etiology of inflammatory diseases, including cardiovascular disease (CVD) and obesity; however, the signaling pathways involved are still under investigation. Dysregulation of the renin-angiotensin system (RAS) can contribute to CVD and alter lipid storage and inflammation in adipose tissue. Our previous exposure studies revealed that traffic-generated emissions increase RAS signaling, further exacerbated by a high-fat diet. Thus, we investigated the hypothesis that exposure to engine emissions increases systemic and local adipocyte RAS signaling, promoting the expression of factors involved in CVD and obesity. Male C57BL/6 mice (6-8 wk old) were fed either a high-fat (HF, n = 16) or low-fat (LF, n = 16) diet, beginning 30d prior to exposures, and then exposed via inhalation to either filtered air (FA, controls) or a mixture of diesel engine + gasoline engine vehicle emissions (MVE: 100 μg PM/m

Indexed as

ACE, angiotensin converting enzymeAdiposeAGT, angiotensinogenAir pollutionAng II, angiotensin IIAT1, angiotensin II receptor subtype 1AT2, angiotensin II receptor subtype 2CVDCVD, cardiovascular diseaseDHE, dihydroethidiumFA, filtered air (controls)GLUT-4, glucose transporter type 4HF, high-fat dietICAM-1, intracellular adhesion molecule-1IL-6, interleukin-6IL-β, interleukin betaIR, insulin receptorLDL, low density lipoproteinLF, low-fat dietLOX-1, lectin-like oxidized low-density lipoprotein receptorMCP-1, monocyte chemoattractant protein-1MOMA-2, anti-monocyte + macrophage antibodyMVE, mixed gasoline and diesel vehicle emissionsObesityPM, particulate matterRAS, renin-angiotensin systemRenin-angiotensin systemROS, reactive oxygen speciesT2D, type 2 diabetesTNF-α, tumor necrosis factor alphaVCAM-1, vascular cell adhesion molecule-1vWF, Von Willebrand factor

Identifiers

PMID33948438
PMCPMC8080412
OpenAlexW3156322464

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.