Evidence map›Paper›PMID 26620549›Full record

ArticleFree radical biology & medicine2016

Nitro-oleic acid modulates classical and regulatory activation of macrophages and their involvement in pro-fibrotic responses.

Gabriela Ambrozova, Hana Martiskova, Adolf Koudelka, Thorben Ravekes, Tanja K Rudolph, Anna Klinke, Volker Rudolph, Bruce A Freeman, Steven R Woodcock, Lukas Kubala and 1 more

Abstract read
In one paragraph

Article in Free radical biology & medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Nitro Fatty Acids (NOMolecules (Basel, Switzerland) · 2021
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. The effect ofVeterinary world · 2020
    Article
  15. Article
  16. Review
  17. Nitrated fatty acids: from diet to disease.Current opinion in physiology · 2019
    Article
  18. Review
  19. Review
  20. 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

11 authors at 5 institutions in 3 countries.

Gabriela Ambrozova *Institute of Biophysics, Academy of Sciences of the Czech Republic, Brno, Czech Republic.
Hana Martiskova *Institute of Biophysics, Academy of Sciences of the Czech Republic, Brno, Czech Republic.
Adolf KoudelkaDepartment of Animal Physiology and Immunology, Masaryk University, Brno, Czech Republic.
Thorben RavekesHeart Centre, University Hospital of Cologne, Cologne, Germany.
Tanja K RudolphHeart Centre, University Hospital of Cologne, Cologne, Germany.
Anna KlinkeHeart Centre, University Hospital of Cologne, Cologne, Germany.
Volker RudolphHeart Centre, University Hospital of Cologne, Cologne, Germany.
Bruce A FreemanDepartment of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, PA, USA.
Steven R WoodcockDepartment of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, PA, USA.
Lukas KubalaInstitute of Biophysics, Academy of Sciences of the Czech Republic, Brno, Czech Republic.
Michaela PekarovaInstitute of Biophysics, Academy of Sciences of the Czech Republic, Brno, Czech Republic.
University Hospital Cologne · DECzech Academy of Sciences · CZMasaryk University · CZUniversity Hospital Brno · CZUniversity of Pittsburgh · US

Funding

Vascular Subphenotypes of Lung DiseaseP01HL103455 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GLADWIN, MARK T · 2011 to 2020
$26.1M
Redox-Derived Pulmonary Anti-Inflammatory MediatorsR01HL064937 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FREEMAN, BRUCE ALAN · 2000 to 2015
$5.6M
Redox Transduction of Nitric Oxide SignalingR37HL058115 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FREEMAN, BRUCE ALAN · 2008 to 2017
$5.2M
NITRIC OXIDE REGULATION OF VASCULAR OXIDANT INJURYR01HL058115 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FREEMAN, BRUCE ALAN · 1998 to 2007
$3.3M
Anti-Inflammatory Lipid Mediators in AsthmaR01HL132550 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FREEMAN, BRUCE ALAN, HOLGUIN, FERNANDO · 2016 to 2019
$2.9M
NHLBI NIH HHS P01 HL103455NHLBI NIH HHS P01-HL-103455NHLBI NIH HHS R01 HL058115NHLBI NIH HHS R01-HL-058115NHLBI NIH HHS R01 HL064937NHLBI NIH HHS R01 HL132550NHLBI NIH HHS R01-HL-64937NHLBI NIH HHS R37 HL058115
6 · The paper itself

Abstract

Inflammation is an immune response triggered by microbial invasion and/or tissue injury. While acute inflammation is directed toward invading pathogens and injured cells, thus enabling tissue regeneration, chronic inflammation can lead to severe pathologies and tissue dysfunction. These processes are linked with macrophage polarization into specific inflammatory "M1-like" or regulatory "M2-like" subsets. Nitro-fatty acids (NO2-FAs), produced endogenously as byproducts of metabolism and oxidative inflammatory conditions, may be useful for treating diseases associated with dysregulated immune homeostasis. The goal of this study was to characterize the role of nitro-oleic acid (OA-NO2) in regulating the functional specialization of macrophages induced by bacterial lipopolysaccharide or interleukin-4, and to reveal specific signaling mechanisms which can account for OA-NO2-dependent modulation of inflammation and fibrotic responses. Our results show that OA-NO2 inhibits lipopolysaccharide-stimulated production of both pro-inflammatory and immunoregulatory cytokines (including transforming growth factor-β) and inhibits nitric oxide and superoxide anion production. OA-NO2 also decreases interleukin-4-induced macrophage responses by inhibiting arginase-I expression and transforming growth factor-β production. These effects are mediated via downregulation of signal transducers and activators of transcription, mitogen-activated protein kinase and nuclear factor-кB signaling responses. Finally, OA-NO2 inhibits fibrotic processes in an in vivo model of angiotensin II-induced myocardial fibrosis by attenuating expression of α-smooth muscle actin, systemic transforming growth factor-β levels and infiltration of both "M1-" and "M2-like" macrophage subsets into afflicted tissue. Overall, the electrophilic fatty acid derivative OA-NO2 modulates a broad range of "M1-" and "M2-like" macrophage functions and represents a potential therapeutic approach to target diseases associated with dysregulated macrophage subsets.

Indexed as

AnimalsCells, CulturedFibrosisInterleukin-4LipopolysaccharidesMacrophage ActivationMiceMice, Inbred C57BLMyocardiumNitric OxideOleic AcidsPPAR gammaSTAT3 Transcription FactorSuperoxides10-nitro-oleic acidInterleukin-4LipopolysaccharidesNitric OxideOleic AcidsPPAR gammaSTAT3 Transcription FactorSuperoxidesFibrosisInflammationMacrophage functional specializationMacrophagesNitro-fatty acidsNitro-oleic acid

Identifiers

PMID26620549
PMCPMC4748956
OpenAlexW2174588307

What OpenQuestion holds

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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.