Evidence map›Paper›PMID 27507404›Full record

ArticleCirculation2016

Resolvin D2 Enhances Postischemic Revascularization While Resolving Inflammation.

Michael J Zhang, Brian E Sansbury, Jason Hellmann, James F Baker, Luping Guo, Caitlin M Parmer, Joshua C Prenner, Daniel J Conklin, Aruni Bhatnagar, Mark A Creager and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Circulation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

64 citing papers in PubMed, 105 citations in OpenAlex.

  1. Plasma Resolvin D2 to Leukotriene BBioMed research international · 2021
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  11. Resolvin D2 limits atherosclerosis progression via myeloid cell-GPR18.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
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4 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

11 authors at 1 institution in 1 country.

Michael J Zhang *Institute of Molecular Cardiology, Diabetes and Obesity Center, Division of Cardiovascular Medicine, University of Louisville School of Medicine, Louisville, KY.
Brian E Sansbury *Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Harvard Institutes of Medicine, Boston, MA.
Jason HellmannCenter for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Harvard Institutes of Medicine, Boston, MA.
James F BakerInstitute of Molecular Cardiology, Diabetes and Obesity Center, Division of Cardiovascular Medicine, University of Louisville School of Medicine, Louisville, KY.
Luping GuoInstitute of Molecular Cardiology, Diabetes and Obesity Center, Division of Cardiovascular Medicine, University of Louisville School of Medicine, Louisville, KY.
Caitlin M ParmerVascular Medicine Section, Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.
Joshua C PrennerVascular Medicine Section, Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.
Daniel J ConklinInstitute of Molecular Cardiology, Diabetes and Obesity Center, Division of Cardiovascular Medicine, University of Louisville School of Medicine, Louisville, KY.
Aruni BhatnagarInstitute of Molecular Cardiology, Diabetes and Obesity Center, Division of Cardiovascular Medicine, University of Louisville School of Medicine, Louisville, KY.
Mark A CreagerVascular Medicine Section, Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.
Matthew SpiteCenter for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Harvard Institutes of Medicine, Boston, MA.
University of Louisville · US

Funding

Resolution Mechanisms in Acute Inflammation: Resolution PharmacologyP01GM095467 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI LEVY, BRUCE D · 2011 to 2020
$14.8M
Project 5 - Metabolomic Analysis of AtherothrombosisP20GM103492 · NIGMS · UNIVERSITY OF LOUISVILLE · PI DEFILIPPIS, ANDREW · 2012 to 2017
$13.8M
Role of Inflammation-Resolving Lipid Mediators In Ischemic RevascularizationR01HL106173 · NHLBI · UNIVERSITY OF LOUISVILLE · PI SPITE, MATTHEW R · 2011 to 2023
$5.7M
Nutrient excess alters resolution of inflammation in diabetes and obesityF32HL116186 · NHLBI · UNIVERSITY OF LOUISVILLE · PI HELLMANN, JASON L · 2013 to 2015
$159k
NHLBI NIH HHS F32 HL116186NHLBI NIH HHS R01 HL106173NIGMS NIH HHS P01 GM095467NIGMS NIH HHS P20 GM103492
6 · The paper itself

Abstract

backgroundResolvins are lipid mediators generated by leukocytes during the resolution phase of inflammation. They have been shown to regulate the transition from inflammation to tissue repair; however, it is unknown whether resolvins play a role in tissue revascularization following ischemia.

methodsWe used a murine model of hind limb ischemia (HLI), coupled with laser Doppler perfusion imaging, microcomputed tomography, and targeted mass spectrometry, to assess the role of resolvins in revascularization and inflammation resolution.

resultsIn mice undergoing HLI, we identified resolvin D2 (RvD2) in bone marrow and skeletal muscle by mass spectrometry (n=4-7 per group). We also identified RvD2 in skeletal muscle biopsies from humans with peripheral artery disease. Monocytes were recruited to skeletal muscle during HLI and isolated monocytes produced RvD2 in a lipoxygenase-dependent manner. Exogenous RvD2 enhanced perfusion recovery in HLI and microcomputed tomography of limb vasculature revealed greater volume, with evidence of tortuous arterioles indicative of arteriogenesis (n=6-8 per group). Unlike other treatment strategies for therapeutic revascularization that exacerbate inflammation, RvD2 did not increase vascular permeability, but reduced neutrophil accumulation and the plasma levels of tumor necrosis factor-α and granulocyte macrophage colony-stimulating factor. In mice treated with RvD2, histopathologic analysis of skeletal muscle of ischemic limbs showed more regenerating myocytes with centrally located nuclei. RvD2 enhanced endothelial cell migration in a Rac-dependent manner, via its receptor, GPR18, and Gpr18-deficient mice had an endogenous defect in perfusion recovery following HLI. Importantly, RvD2 rescued defective revascularization in diabetic mice.

conclusionsRvD2 stimulates arteriogenic revascularization during HLI, suggesting that resolvins may be a novel class of mediators that both resolve inflammation and promote arteriogenesis.

Indexed as

AnimalsCells, CulturedCohort StudiesDocosahexaenoic AcidsFemaleHindlimbHumansInflammationIschemiaMaleMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutMice, ObeseMiddle AgedDocosahexaenoic Acidsresolvin D2imaging techniquesinflammationperipheral vascular diseasesrevascularization

Identifiers

PMID27507404
PMCPMC5214591
OpenAlexW2516378834

What OpenQuestion holds

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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.