Evidence map›Paper›PMID 23564731›Full record

ArticleJournal of lipid research2013

Ambient ultrafine particles alter lipid metabolism and HDL anti-oxidant capacity in LDLR-null mice.

Rongsong Li, Mohamad Navab, Payam Pakbin, Zhi Ning, Kaveh Navab, Greg Hough, Todd E Morgan, Caleb E Finch, Jesus A Araujo, Alan M Fogelman and 2 more

Abstract read
In one paragraph

Article in Journal of lipid research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

53 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Association between PMFrontiers in public health · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Longitudinal associations between ambient PMEnvironmental epidemiology (Philadelphia, Pa.) · 2024
    Article
  11. Article
  12. Article
  13. Personal exposure of PMEnvironmental science and pollution research international · 2023
    Observational
  14. Review
  15. Article
  16. Air Pollution: Another Threat to HDL Function.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Article
  19. Article
  20. Review
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

12 authors.

Rongsong LiDepartment of Biomedical Engineering, University of Southern California, Los Angeles, CA; Division of Cardiology, Department of Medicine, University of California, Los Angeles School of Medicine, Los Angeles, CA; and.
Mohamad NavabDivision of Cardiology, Department of Medicine, University of California, Los Angeles School of Medicine, Los Angeles, CA; and.
Payam PakbinDepartment of Civil Engineering and Environmental Science, and University of Southern California, Los Angeles, CA.
Zhi NingSchool of Energy and Environment, City University of Hong Kong, Hong Kong.
Kaveh NavabDivision of Cardiology, Department of Medicine, University of California, Los Angeles School of Medicine, Los Angeles, CA; and.
Greg HoughDivision of Cardiology, Department of Medicine, University of California, Los Angeles School of Medicine, Los Angeles, CA; and.
Todd E MorganDavis School of Gerontology, University of Southern California, Los Angeles, CA.
Caleb E FinchDavis School of Gerontology, University of Southern California, Los Angeles, CA.
Jesus A AraujoDivision of Cardiology, Department of Medicine, University of California, Los Angeles School of Medicine, Los Angeles, CA; and.
Alan M FogelmanDivision of Cardiology, Department of Medicine, University of California, Los Angeles School of Medicine, Los Angeles, CA; and.
Constantinos SioutasDepartment of Civil Engineering and Environmental Science, and University of Southern California, Los Angeles, CA.
Tzung HsiaiDepartment of Biomedical Engineering, University of Southern California, Los Angeles, CA; Division of Cardiology, Department of Medicine, University of California, Los Angeles School of Medicine, Los Angeles, CA; and. Electronic address: hsiai@usc.edu.

Funding

ULTRASTRUCTURE OF THE INTIMA IN EARLY LESION FORMATIONP01HL030568 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FOGELMAN, ALAN M · 1985 to 2019
$55.2M
Linking Spatial Variations Shear Stress-Oxidative StressR01HL083015 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HSIAI, TZUNG K · 2006 to 2015
$3.9M
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
Shear Stress and Mechnaically Unstable PlaqueR21HL091302 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HSIAI, TZUNG K · 2009 to 2010
$432k
Air Pollution and vulnerability to Alzheimer-like neurodegeneration in miceR21AG040683 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI FINCH, CALEB E · 2011 to 2012
$365k
Aging and sensitivity to traffic-generated air pollutants in male and female miceR21AG040753 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI FINCH, CALEB E · 2011 to 2012
$365k
NHLBI NIH HHS P01 HL030568NHLBI NIH HHS P0HL-030568NHLBI NIH HHS R01 HL083015NHLBI NIH HHS R01HL-083015NHLBI NIH HHS R21 HL091302NHLBI NIH HHS R21HL-091302NIA NIH HHS R21 AG040683NIA NIH HHS R21 AG040753NIEHS NIH HHS R01 ES016959NIEHS NIH HHS R01ES-016959
6 · The paper itself

Abstract

Exposure to ambient particulate matter (PM) is a risk factor for cardiovascular diseases. The redox-active ultrafine particles (UFPs) promote vascular oxidative stress and inflammatory responses. We hypothesized that UFPs modulated lipid metabolism and anti-oxidant capacity of high density lipoprotein (HDL) with an implication in atherosclerotic lesion size. Fat-fed low density lipoprotein receptor-null (LDLR⁻/⁻ mice were exposed to filtered air (FA) or UFPs for 10 weeks with or without administering an apolipoprotein A-I mimetic peptide made of D-amino acids, D-4F. LDLR⁻/⁻ mice exposed to UFPs developed a reduced plasma HDL level (P < 0.01), paraoxonase activity (P < 0.01), and HDL anti-oxidant capacity (P < 0.05); but increased LDL oxidation, free oxidized fatty acids, triglycerides, serum amyloid A (P < 0.05), and tumor necrosis factor α (P < 0.05), accompanied by a 62% increase in the atherosclerotic lesion ratio of the en face aortic staining and a 220% increase in the cross-sectional lesion area of the aortic sinus (P < 0.001). D-4F administration significantly attenuated these changes. UFP exposure promoted pro-atherogenic lipid metabolism and reduced HDL anti-oxidant capacity in fat-fed LDLR⁻/⁻ mice, associated with a greater atherosclerotic lesion size compared with FA-exposed animals. D-4F attenuated UFP-mediated pro-atherogenic effects, suggesting the role of lipid oxidation underlying UFP-mediated atherosclerosis.

Indexed as

Receptors, LDLAnimalsAntioxidantsApolipoprotein A-IAtherosclerosisDietary FatsLipid MetabolismLipoproteins, HDLMiceMice, KnockoutOxidation-ReductionParticulate MatterPeptidomimeticsAntioxidantsApolipoprotein A-ID-4F peptideDietary FatsLipoproteins, HDLParticulate MatterPeptidomimeticsReceptors, LDLatherosclerosisD-4Fhigh density lipoproteinlow density lipoprotein receptor-null

Identifiers

PMID23564731
PMCPMC3646462

What OpenQuestion holds

Textmetadata
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.