Evidence map›Paper›PMID 31159424›Full record

ReviewInternational journal of molecular sciences2019

Akt Signaling in Macrophage Polarization, Survival, and Atherosclerosis.

MacRae F Linton, Javid J Moslehi, Vladimir R Babaev

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed, 3 pooled it
8.9field-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

158 citing papers in PubMed, 3 syntheses or guidelines pooled it, 269 citations in OpenAlex.

  1. Pooled it
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  4. Review
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  12. Distinct types of regulated cell death in atherosclerosis.Journal of pharmaceutical analysis · 2026
    Review
  13. Comparative Immunomodulatory Profiles ofJournal of microbiology and biotechnology · 2026
    Article
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98 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

3 authors at 1 institution in 1 country.

MacRae F LintonAtherosclerosis Research Unit, Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University School of Medicine, 2220 Pierce Avenue, Nashville, TN 37232-6300, USA. macrae.linton@vumc.org.
Javid J MoslehiAtherosclerosis Research Unit, Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University School of Medicine, 2220 Pierce Avenue, Nashville, TN 37232-6300, USA. javid.moslehi@vumc.org.
Vladimir R BabaevAtherosclerosis Research Unit, Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University School of Medicine, 2220 Pierce Avenue, Nashville, TN 37232-6300, USA. vladimir.babaev@vumc.org.
Vanderbilt University · US

Funding

Non-coding RNA & Bioinformatics CoreP01HL116263 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI LINTON, MACRAE F · 2014 to 2025
$24.7M
ApoE and SR-BI as Determinants of HDL and Macrophage Function in AtherogenesisR01HL086988 · NHLBI · VANDERBILT UNIVERSITY · PI LINTON, MACRAE F · 2007 to 2010
$1.5M
NHLBI NIH HHS P01 HL116263NHLBI NIH HHS R01 HL086988
6 · The paper itself

Abstract

The PI3K/Akt pathway plays a crucial role in the survival, proliferation, and migration of macrophages, which may impact the development of atherosclerosis. Changes in Akt isoforms or modulation of the Akt activity levels in macrophages significantly affect their polarization phenotype and consequently atherosclerosis in mice. Moreover, the activity levels of Akt signaling determine the viability of monocytes/macrophages and their resistance to pro-apoptotic stimuli in atherosclerotic lesions. Therefore, elimination of pro-apoptotic factors as well as factors that antagonize or suppress Akt signaling in macrophages increases cell viability, protecting them from apoptosis, and this markedly accelerates atherosclerosis in mice. In contrast, inhibition of Akt signaling by the ablation of Rictor in myeloid cells, which disrupts mTORC2 assembly, significantly decreases the viability and proliferation of blood monocytes and macrophages with the suppression of atherosclerosis. In addition, monocytes and macrophages exhibit a threshold effect for Akt protein levels in their ability to survive. Ablation of two Akt isoforms, preserving only a single Akt isoform in myeloid cells, markedly compromises monocyte and macrophage viability, inducing monocytopenia and diminishing early atherosclerosis. These recent advances in our understanding of Akt signaling in macrophages in atherosclerosis may have significant relevance in the burgeoning field of cardio-oncology, where PI3K/Akt inhibitors being tested in cancer patients can have significant cardiovascular and metabolic ramifications.

Indexed as

Signal TransductionAnimalsApoptosisAtherosclerosisBlood CellsCell SurvivalHumansMacrophage ActivationMacrophagesPhosphatidylinositol 3-KinasesProtein IsoformsProto-Oncogene Proteins c-aktPhosphatidylinositol 3-KinasesProtein IsoformsProto-Oncogene Proteins c-aktAkt signalingapoptosisatherosclerosismacrophagespolarizationsurvival

Identifiers

PMID31159424
PMCPMC6600269
OpenAlexW2947325783

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.