Evidence map›Paper›PMID 30846875›Full record

ReviewNature reviews. Cardiology2019

Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities.

Magnus Bäck, Arif Yurdagul, Ira Tabas, Katariina Öörni, Petri T Kovanen

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07331103 (RESOLving INflammation Through Diet for Health Multicenter, Prospective Randomized, Controlled and Open- Label to Examine the Impact of a Diet Enriched in Omega 3 Fatty Acids of Animal and Vegetal Origin on Circulating Lipid-driven Pro-/Antiinflammatory Balance in Subjects at Moderate to High Cardiovascular Risk.), which is not on this map. Cited by 808 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
808citing papers in PubMed, 3 pooled it
101.2field-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.

NCT07331103 narecruitingnot on this mapstarted 2025, after this paper: background citation

RESOLving INflammation Through Diet for Health Multicenter, Prospective Randomized, Controlled and Open- Label to Examine the Impact of a Diet Enriched in Omega 3 Fatty Acids of Animal and Vegetal Origin on Circulating Lipid-driven Pro-/Antiinflammatory Balance in Subjects at Moderate to High Cardiovascular Risk.

TypeinterventionalSponsorMario Negri Institute for Pharmacological ResearchRan2025 to 2026Enrolled324ConditionsCardiovascualr Disease, Lipids, Inflammation, n-3 Polyunsatured Fatty Acids (n-3 PUFA)ArmsFish Oil, Camelina oil, Vitamin E
3 · Its place in the literature

Who cites it

808 citing papers in PubMed, 3 syntheses or guidelines pooled it, 1,298 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

748 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

5 authors at 4 institutions in 3 countries.

Magnus BäckDepartment of Cardiology, Karolinska University Hospital, Stockholm, Sweden.
Arif YurdagulColumbia University Irving Medical Center, New York, NY, USA.
Ira TabasColumbia University Irving Medical Center, New York, NY, USA.
Katariina ÖörniAtherosclerosis Research Laboratory, Wihuri Research Institute, Helsinki, Finland.
Petri T KovanenAtherosclerosis Research Laboratory, Wihuri Research Institute, Helsinki, Finland. petri.kovanen@wri.fi.
Columbia University Irving Medical Center · USKarolinska University Hospital · SEUniversity of Helsinki · FIWihuri Research Institute · FI

Funding

TTC39B in obesity and atherosclerosisP01HL087123 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TALL, ALAN RICHARD · 2007 to 2022
$31.2M
POSTDOCTORAL TRAINING IN ARTERIOSCLEROSIS RESEARCHT32HL007343 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI HENRY N GINSBERG, Muredach P Reilly · 1985 to 2026
$12.7M
A Mechanistic and Translational Research Program Linking Impaired Resolution, Defective Efferocytosis, and Clonal Hematopoiesis to the Formation of Clinically Dangerous Atherosclerotic PlaquesR35HL145228 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2019 to 2025
$6.8M
The Unfolded Protein Response in Sterol CytoxicityR01HL075662 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2004 to 2017
$5.6M
Enhancing Inflammation Resolution in Atherosclerosis via Targeted Nanoparticle-Mediated Delivery of BiologicsR01HL127464 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SHI, JINJUN, TABAS, IRA A · 2016 to 2019
$3.0M
Mechanisms of Defective Efferocytosis in AtherosclerosisR01HL107497 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2012 to 2015
$1.6M
"MerTK Cleavage and Signaling in Atherosclerosis"R01HL132412 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2016 to 2018
$1.5M
Processing of Apoptotic Cell-Derived Cargo by Macrophages Continues Efferocytosis and Drives Atherosclerosis RegressionK99HL145131 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI YURDAGUL, ARIF · 2019 to 2020
$335k
CaMKII/MK2 Signaling in Cardiometabolic DiseaseR01HL140554 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2018 to 2018
$138k
NHLBI NIH HHS K99 HL145131NHLBI NIH HHS P01 HL087123NHLBI NIH HHS R01 HL075662NHLBI NIH HHS R01 HL107497NHLBI NIH HHS R01 HL127464NHLBI NIH HHS R01 HL132412NHLBI NIH HHS R01 HL140554NHLBI NIH HHS R35 HL145228NHLBI NIH HHS T32 HL007343
6 · The paper itself

Abstract

Atherosclerosis is a lipid-driven inflammatory disease of the arterial intima in which the balance of pro-inflammatory and inflammation-resolving mechanisms dictates the final clinical outcome. Intimal infiltration and modification of plasma-derived lipoproteins and their uptake mainly by macrophages, with ensuing formation of lipid-filled foam cells, initiate atherosclerotic lesion formation, and deficient efferocytotic removal of apoptotic cells and foam cells sustains lesion progression. Defective efferocytosis, as a sign of inadequate inflammation resolution, leads to accumulation of secondarily necrotic macrophages and foam cells and the formation of an advanced lesion with a necrotic lipid core, indicative of plaque vulnerability. Resolution of inflammation is mediated by specialized pro-resolving lipid mediators derived from omega-3 fatty acids or arachidonic acid and by relevant proteins and signalling gaseous molecules. One of the major effects of inflammation resolution mediators is phenotypic conversion of pro-inflammatory macrophages into macrophages that suppress inflammation and promote healing. In advanced atherosclerotic lesions, the ratio between specialized pro-resolving mediators and pro-inflammatory lipids (in particular leukotrienes) is strikingly low, providing a molecular explanation for the defective inflammation resolution features of these lesions. In this Review, we discuss the mechanisms of the formation of clinically dangerous atherosclerotic lesions and the potential of pro-resolving mediator therapy to inhibit this process.

Indexed as

AnimalsApoptosisAtherosclerosisHumansInflammasomesInflammationLipid MetabolismLipoproteinsMacrophagesNLR Family, Pyrin Domain-Containing 3 ProteinSignal TransductionTunica IntimaInflammasomesLipoproteinsNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, human

Identifiers

PMID30846875
PMCPMC6727648
OpenAlexW2920248606

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.