Evidence map›Paper›PMID 29379788›Full record

ReviewFrontiers in cardiovascular medicine2017

Mechanisms and Consequences of Defective Efferocytosis in Atherosclerosis.

Arif Yurdagul, Amanda C Doran, Bishuang Cai, Gabrielle Fredman, Ira A Tabas

Abstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
187citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

187 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
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  7. Article
  8. Review
  9. Protectin D1/GPR37 Signaling Enhances Macrophage-Dependent Efferocytosis to Attenuate Experimental Abdominal Aortic Aneurysm Formation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
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  16. More Than a Cleanup Crew: The Expanding Biology of Efferocytosis.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  17. Review
  18. Review
  19. Review
  20. Review

127 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.

Arif YurdagulDepartment of Medicine, Columbia University, New York, NY, United States.
Amanda C DoranDepartment of Medicine, Columbia University, New York, NY, United States.
Bishuang CaiDepartment of Medicine, Columbia University, New York, NY, United States.
Gabrielle FredmanDepartment of Molecular and Cellular Physiology, Albany Medical College, Albany, NY, United States.
Ira A TabasDepartment of Medicine, Columbia University, New York, NY, United States.

Funding

TTC39B in obesity and atherosclerosisP01HL087123 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 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
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
CaMKII/MK2 Signaling in Cardiometabolic DiseaseR01HL140554 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2018 to 2018
$138k
NHLBI NIH HHS P01 HL087123NHLBI NIH HHS R00 HL119587NHLBI NIH HHS R01 HL075662NHLBI NIH HHS R01 HL127464NHLBI NIH HHS R01 HL132412NHLBI NIH HHS R01 HL140554NHLBI NIH HHS T32 HL007343
6 · The paper itself

Abstract

Efficient clearance of apoptotic cells, termed efferocytosis, critically regulates normal homeostasis whereas defective uptake of apoptotic cells results in chronic and non-resolving inflammatory diseases, such as advanced atherosclerosis. Monocyte-derived macrophages recruited into developing atherosclerotic lesions initially display efficient efferocytosis and temper inflammatory responses, processes that restrict plaque progression. However, during the course of plaque development, macrophages undergo cellular reprogramming that reduces efferocytic capacity, which results in post-apoptotic necrosis of apoptotic cells and inflammation. Furthermore, defective efferocytosis in advanced atherosclerosis is a major driver of necrotic core formation, which can trigger plaque rupture and acute thrombotic cardiovascular events. In this review, we discuss the molecular and cellular mechanisms that regulate efferocytosis, how efferocytosis promotes the resolution of inflammation, and how defective efferocytosis leads to the formation of clinically dangerous atherosclerotic plaques.

Indexed as

atherosclerosisefferocytosisinflammation resolutionmacrophagespost-apoptotic necrosis

Identifiers

PMID29379788
PMCPMC5770804

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.