Evidence map›Paper›PMID 27725526›Full record

ReviewCirculation journal : official journal of the Japanese Circulation Society2016

Macrophage Apoptosis and Efferocytosis in the Pathogenesis of Atherosclerosis.

MacRae F Linton, Vladimir R Babaev, Jiansheng Huang, Edward F Linton, Huan Tao, Patricia G Yancey

Open access · diamondAbstract readReview
In one paragraph

Review in Circulation journal : official journal of the Japanese Circulation Society, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
134citing papers in PubMed, 2 pooled it
7.3field-weighted citation impact, top 2% 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

134 citing papers in PubMed, 2 syntheses or guidelines pooled it, 224 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  7. Article
  8. Targeting PANoptosis in atherosclerosis: bridging cell death mechanisms and therapy.Apoptosis : an international journal on programmed cell death · 2026
    Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Efferocytosis: The Silent Guardian of Tissue Homeostasis and Cardiovascular Health.Journal of cardiovascular development and disease · 2025
    Review
  14. Foods (Basel, Switzerland) · 2025
    Article
  15. GATA2 Mediates Macrophage Proliferation During Atherosclerosis.Journal of the American Heart Association · 2025
    Article
  16. Review
  17. Review
  18. Article
  19. TIPE2: a novel regulatory factor for cardiovascular-related diseases.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
  20. Article

74 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

6 authors at 2 institutions in 1 country.

MacRae F LintonAtherosclerosis Research Unit, Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center.
Vladimir R Babaev
Jiansheng Huang
Edward F Linton
Huan Tao
Patricia G Yancey
Vanderbilt University Medical Center · USUniversity of Pennsylvania · US

Funding

Non-coding RNA & Bioinformatics CoreP01HL116263 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI DAVIES, SEAN STEPHEN · 2014 to 2025
$24.7M
Macrophage SR-BI Regulates Autophagy, Angiogenin and tRNA-derived small RNAsR01HL127173 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI LINTON, MACRAE F, VICKERS, KASEY C · 2016 to 2019
$2.1M
Macrophage Akt and IKKalpha signaling in apoptosis and atherosclerosisR01HL105375 · NHLBI · VANDERBILT UNIVERSITY · PI LINTON, MACRAE F · 2010 to 2013
$1.8M
Mechanisms for Dysfunctional HDL Formation in Familial HypercholesterolemiaR01HL111945 · NHLBI · VANDERBILT UNIVERSITY · PI LINTON, MACRAE F · 2012 to 2013
$920k
NHLBI NIH HHS P01 HL116263NHLBI NIH HHS R01 HL105375NHLBI NIH HHS R01 HL111945NHLBI NIH HHS R01 HL127173
6 · The paper itself

Abstract

Macrophage apoptosis and the ability of macrophages to clean up dead cells, a process called efferocytosis, are crucial determinants of atherosclerosis lesion progression and plaque stability. Environmental stressors initiate endoplasmic reticulum (ER) stress and activate the unfolded protein response (UPR). Unresolved ER stress with activation of the UPR initiates apoptosis. Macrophages are resistant to apoptotic stimuli, because of activity of the PI3K/Akt pathway. Macrophages express 3 Akt isoforms, Akt1, Akt2 and Akt3, which are products of distinct but homologous genes. Akt displays isoform-specific effects on atherogenesis, which vary with different vascular cell types. Loss of macrophage Akt2 promotes the anti-inflammatory M2 phenotype and reduces atherosclerosis. However, Akt isoforms are redundant with regard to apoptosis. c-Jun NH

Indexed as

Endoplasmic Reticulum StressSignal TransductionUnfolded Protein ResponseAnimalsAtherosclerosisHumansI-kappa B KinaseIsoenzymesMacrophagesMechanistic Target of Rapamycin Complex 2Mitogen-Activated Protein Kinase 8Multiprotein ComplexesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesI-kappa B KinaseIsoenzymesMechanistic Target of Rapamycin Complex 2Mitogen-Activated Protein Kinase 8Multiprotein ComplexesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID27725526
PMCPMC5459487
OpenAlexW2527981400

What OpenQuestion holds

Textmetadata
LicenceTDM
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.