Evidence map›Paper›PMID 28527709›Full record

ReviewThe American journal of pathology2017

Boosting Inflammation Resolution in Atherosclerosis: The Next Frontier for Therapy.

Gabrielle Fredman, Ira Tabas

Open access · bronzeAbstract readReview
In one paragraph

Review in The American journal of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed
12.9field-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

103 citing papers in PubMed, 166 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
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  12. Inulin may inhibit ADAM17 to delay atherosclerosis.Open medicine (Warsaw, Poland) · 2026
    Article
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  15. Metabolic reprogramming in efferocytosis.Frontiers in cell and developmental biology · 2025
    Review
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  20. Article

43 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

2 authors at 2 institutions in 1 country.

Gabrielle FredmanDepartment of Molecular and Cellular Physiology, Center for Cardiovascular Sciences, Albany Medical College, Albany, New York. Electronic address: fredmag@mail.amc.edu.
Ira TabasDepartments of Medicine, Pathology and Cell Biology, and Physiology, Columbia University Medical Center, New York, New York.
Albany Medical Center Hospital · USColumbia University Irving Medical Center · US

Funding

TTC39B in obesity and atherosclerosisP01HL087123 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 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
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
Specialized pro-resolving mediators in atherosclerosisR00HL119587 · NHLBI · ALBANY MEDICAL COLLEGE · PI FREDMAN, GABRIELLE · 2015 to 2017
$731k
Specialized pro-resolving mediators in atherosclerosisK99HL119587 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI FREDMAN, GABRIELLE · 2013 to 2014
$216k
CaMKII/MK2 Signaling in Cardiometabolic DiseaseR01HL140554 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2018 to 2018
$138k
NHLBI NIH HHS K99 HL119587NHLBI NIH HHS P01 HL087123NHLBI NIH HHS R00 HL119587NHLBI NIH HHS R01 HL075662NHLBI NIH HHS R01 HL127464NHLBI NIH HHS R01 HL132412NHLBI NIH HHS R01 HL140554
6 · The paper itself

Abstract

Defective inflammation resolution is the underlying cause of prevalent chronic inflammatory diseases, such as arthritis, asthma, cancer, and neurodegenerative and cardiovascular diseases. Inflammation resolution is governed by several endogenous factors, including fatty acid-derived specialized proresolving mediators and proteins, such as annexin A1. Specifically, specialized proresolving mediators comprise a family of mediators that include arachidonic acid-derived lipoxins, omega-3 fatty acid eicosapentaenoic acid-derived resolvins, docosahexaenoic acid-derived resolvins, protectins, and maresins. Emerging evidence indicates that imbalances between specialized proresolving mediators and proinflammatory mediators are associated with several prevalent human diseases, including atherosclerosis. Mechanisms that drive this imbalance remain largely unknown and will be discussed in this review. Furthermore, the concept of dysregulated inflammation resolution in atherosclerosis has been known for several decades. Recently, there has been an explosion of new work with regard to the therapeutic application of proresolving ligands in experimental atherosclerosis. Therefore, this review will highlight recent advances in our understanding of how inflammation resolution may become defective in atherosclerosis and the potential for proresolving therapeutics in atherosclerosis. Last, we offer insight for future implications of the field.

Indexed as

AnimalsAnti-Inflammatory AgentsAtherosclerosisCollagenDisease ProgressionHumansImmunologic FactorsInflammationInflammation MediatorsMolecular Targeted TherapyPlaque, AtheroscleroticRegenerationWound HealingAnti-Inflammatory AgentsCollagenImmunologic FactorsInflammation Mediators

Identifiers

PMID28527709
PMCPMC5455064
OpenAlexW2616120362

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.