Evidence map›Paper›PMID 30108191›Full record

ReviewThe Journal of clinical investigation2018

The role of non-resolving inflammation in atherosclerosis.

Canan Kasikara, Amanda C Doran, Bishuang Cai, Ira Tabas

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
147citing papers in PubMed, 4 pooled it
17.3field-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

147 citing papers in PubMed, 4 syntheses or guidelines pooled it, 256 citations in OpenAlex.

  1. Pooled it
  2. Cardiovascular events risk in patients with systemic autoimmune diseases: a prognostic systematic review and meta-analysis.Clinical research in cardiology : official journal of the German Cardiac Society · 2024
    Pooled it
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  5. 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
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  19. Network Medicine-Based Repurposing of Mesalazine for Atherosclerosis Treatment.Journal of cardiovascular translational research · 2025
    Article
  20. Identification of Myeloid Protein Kinase C Epsilon as a Novel Atheroprotective Gene.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Article

87 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

4 authors at 1 institution in 2 countries.

Canan KasikaraDepartment of Medicine.
Amanda C DoranDepartment of Medicine.
Bishuang CaiDepartment of Medicine.
Ira TabasDepartment of Medicine.
Czech Academy of Sciences, Institute of Physiology · CZ

Funding

TTC39B in obesity and atherosclerosisP01HL087123 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TALL, ALAN RICHARD · 2007 to 2022
$31.2M
The Unfolded Protein Response in Sterol CytoxicityR01HL075662 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2004 to 2017
$5.6M
Training in Cardiovascular Translational ResearchT32HL120826 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MARKS, ANDREW ROBERT, TABAS, IRA A · 2014 to 2023
$4.7M
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
"MerTK Cleavage and Signaling in Atherosclerosis"R01HL132412 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2016 to 2018
$1.5M
NHLBI NIH HHS P01 HL087123NHLBI NIH HHS R01 HL075662NHLBI NIH HHS R01 HL127464NHLBI NIH HHS R01 HL132412NHLBI NIH HHS T32 HL120826
6 · The paper itself

Abstract

Non-resolving inflammation drives the development of clinically dangerous atherosclerotic lesions by promoting sustained plaque inflammation, large necrotic cores, thin fibrous caps, and thrombosis. Resolution of inflammation is not merely a passive return to homeostasis, but rather an active process mediated by specific molecules, including fatty acid-derived specialized pro-resolving mediators (SPMs). In advanced atherosclerosis, there is an imbalance between levels of SPMs and proinflammatory lipid mediators, which results in sustained leukocyte influx into lesions, inflammatory macrophage polarization, and impaired efferocytosis. In animal models of advanced atherosclerosis, restoration of SPMs limits plaque progression by suppressing inflammation, enhancing efferocytosis, and promoting an increase in collagen cap thickness. This Review discusses the roles of non-resolving inflammation in atherosclerosis and highlights the unique therapeutic potential of SPMs in blocking the progression of clinically dangerous plaques.

Indexed as

AnimalsAtherosclerosisDisease ProgressionHumansInflammationInflammation MediatorsLipid MetabolismLipoxygenasesModels, CardiovascularPlaque, AtheroscleroticSignal TransductionInflammation MediatorsLipoxygenases

Identifiers

PMID30108191
PMCPMC6025992
OpenAlexW2809703637

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.