Evidence map›Paper›PMID 25792445›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2015

Resolvin E1 (RvE1) Attenuates Atherosclerotic Plaque Formation in Diet and Inflammation-Induced Atherogenesis.

Hatice Hasturk, Rima Abdallah, Alpdogan Kantarci, Daniel Nguyen, Nicholas Giordano, James Hamilton, Thomas E Van Dyke

Open access · bronzeAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed
15.4field-weighted citation impact, top 1% 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

120 citing papers in PubMed, 195 citations in OpenAlex.

  1. Lipoxins modulate neutrophil oxidative burst, integrin expression and lymphatic transmigration differentially in human health and atherosclerosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Trial
  2. Trial
  3. Specialized proresolving lipid mediators in patients with coronary artery disease and their potential for clot remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Trial
  4. Article
  5. Article
  6. Review
  7. Review
  8. Impacts of Oxylipins on ischemic stroke: from pathophysiology to clinical phenotypes.Metabolomics : Official journal of the Metabolomic Society · 2025
    Review
  9. Anti-Atherogenic Mechanisms and Therapies.Current atherosclerosis reports · 2025
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. "A Time to Tear Down and a Time to Mend": The Role of Eicosanoids in Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2024
    Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Omega-3 (Nutrients · 2024
    Review

60 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 2 countries.

Hatice HasturkFrom the Department of Applied Oral Sciences, Center for Periodontology, The Forsyth Institute, Cambridge, MA (H.H., A.K., D.N., T.E.V.D.); Department of Biological and Diagnostic Sciences, Beirut Arab University, Beirut, Lebanon (R.A.); Department of Biophysics, Boston University School of Medicine, MA (J.H.); and Department of Biomedical Engineering, Boston University, MA (N.G.). hhasturk@forsyth.org tvandyke@forsyth.org.
Rima AbdallahFrom the Department of Applied Oral Sciences, Center for Periodontology, The Forsyth Institute, Cambridge, MA (H.H., A.K., D.N., T.E.V.D.); Department of Biological and Diagnostic Sciences, Beirut Arab University, Beirut, Lebanon (R.A.); Department of Biophysics, Boston University School of Medicine, MA (J.H.); and Department of Biomedical Engineering, Boston University, MA (N.G.).
Alpdogan KantarciFrom the Department of Applied Oral Sciences, Center for Periodontology, The Forsyth Institute, Cambridge, MA (H.H., A.K., D.N., T.E.V.D.); Department of Biological and Diagnostic Sciences, Beirut Arab University, Beirut, Lebanon (R.A.); Department of Biophysics, Boston University School of Medicine, MA (J.H.); and Department of Biomedical Engineering, Boston University, MA (N.G.).
Daniel NguyenFrom the Department of Applied Oral Sciences, Center for Periodontology, The Forsyth Institute, Cambridge, MA (H.H., A.K., D.N., T.E.V.D.); Department of Biological and Diagnostic Sciences, Beirut Arab University, Beirut, Lebanon (R.A.); Department of Biophysics, Boston University School of Medicine, MA (J.H.); and Department of Biomedical Engineering, Boston University, MA (N.G.).
Nicholas GiordanoFrom the Department of Applied Oral Sciences, Center for Periodontology, The Forsyth Institute, Cambridge, MA (H.H., A.K., D.N., T.E.V.D.); Department of Biological and Diagnostic Sciences, Beirut Arab University, Beirut, Lebanon (R.A.); Department of Biophysics, Boston University School of Medicine, MA (J.H.); and Department of Biomedical Engineering, Boston University, MA (N.G.).
James HamiltonFrom the Department of Applied Oral Sciences, Center for Periodontology, The Forsyth Institute, Cambridge, MA (H.H., A.K., D.N., T.E.V.D.); Department of Biological and Diagnostic Sciences, Beirut Arab University, Beirut, Lebanon (R.A.); Department of Biophysics, Boston University School of Medicine, MA (J.H.); and Department of Biomedical Engineering, Boston University, MA (N.G.).
Thomas E Van DykeFrom the Department of Applied Oral Sciences, Center for Periodontology, The Forsyth Institute, Cambridge, MA (H.H., A.K., D.N., T.E.V.D.); Department of Biological and Diagnostic Sciences, Beirut Arab University, Beirut, Lebanon (R.A.); Department of Biophysics, Boston University School of Medicine, MA (J.H.); and Department of Biomedical Engineering, Boston University, MA (N.G.). hhasturk@forsyth.org tvandyke@forsyth.org.
Beirut Arab University · LBBoston University · US

Funding

Specialized Center for Oral Inflammation and ResolutionP50DE016191 · NIDCR · BRIGHAM AND WOMEN'S HOSPITAL · PI SERHAN, CHARLES NICHOLAS · 2004 to 2010
$13.6M
Neutrophils and Periodontitis in DiabetesR01DE015566 · NIDCR · BOSTON UNIVERSITY MEDICAL CAMPUS · PI VAN DYKE, THOMAS ELLIOTT · 2005 to 2014
$4.2M
Novel Mechanisms in Resolution to Harness Inflammation for ReconstructionR01DE019938 · NIDCR · BRIGHAM AND WOMEN'S HOSPITAL · PI IRIMIA, DANIEL, SERHAN, CHARLES NICHOLAS · 2009 to 2012
$2.7M
Treatment of Periodontitis and Inflammatory Changes in DiabetesK23DE018917 · NIDCR · BOSTON UNIVERSITY MEDICAL CAMPUS · PI HASTURK, HATICE · 2008 to 2012
$647k
NIDCR NIH HHS DE15566NIDCR NIH HHS DE18917NIDCR NIH HHS DE19938NIDCR NIH HHS K23 DE018917NIDCR NIH HHS P50 DE016191NIDCR NIH HHS R01 DE015566NIDCR NIH HHS R01 DE019938
6 · The paper itself

Abstract

objectiveEpidemiological and recent clinical studies implicate periodontitis as an independent risk factor for cardiovascular disease. Previously, we demonstrated that rabbits with experimental periodontitis and cholesterol diet exhibit more aortic plaque compared with diet alone. We also showed that a proresolution mediator, Resolvin E1 (RvE1), reverses the experimental periodontitis. Here, we determined whether oral/topical application of RvE1 attenuates aortic atherosclerosis induced by both diet and periodontal inflammation. APPROACH AND

resultsThirty-nine rabbits on a 13-week regimen of 0.5% cholesterol diet were included. Periodontitis was induced by Porphyromonas gingivalis in 24 rabbits and 15 rabbits were placed in no-periodontitis groups. Interventions were no-treatment, vehicle, and RvE1 treatment (4 μg/site or 0.4 μg/site) topically applied 3× per week. At 13 weeks, both periodontitis and atherosclerosis were quantified. Atherosclerotic plaques were assessed by Sudan IV staining, histology, and ex vivo MRI. Serum levels of C-reactive protein were evaluated as a measure of systemic inflammation. RvE1, used as an oral/topical agent, significantly diminished atherogenesis and prevented periodontitis (P<0.05). In the absence of periodontal inflammation, oral/topical application of RvE1 resulted in significantly less arterial plaque, a lower intima/media ratio, and decreased inflammatory cell infiltration compared with no-treatment (P<0.001). Local oral RvE1 application significantly reduced systemic levels of C-reactive protein (P<0.05).

conclusionsThe results suggest that oral/topical RvE1 attenuates enhanced atherogenesis induced by periodontitis and prevents vascular inflammation and atherogenesis in the absence of periodontitis. The inhibition of vascular inflammation with endogenous mediators of resolution of inflammation provides a novel approach in the prevention of atherogenic events.

Indexed as

Diet, AtherogenicAdministration, TopicalAnimalsAtherosclerosisBiopsy, NeedleC-Reactive ProteinDisease Models, AnimalEicosapentaenoic AcidImmunohistochemistryInflammationMalePeriodontitisRabbitsRandom AllocationReference ValuesRisk Assessment5S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acidC-Reactive ProteinEicosapentaenoic Acidatherosclerosisinflammationmodels, animal

Identifiers

PMID25792445
PMCPMC4415167
OpenAlexW2099005050

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.