Evidence map›Paper›PMID 34290249›Full record

ArticleNature communications2021

Role of Tim4 in the regulation of ABCA1

M S Magalhaes, P Smith, J R Portman, L H Jackson-Jones, C C Bain, P Ramachandran, Z Michailidou, R H Stimson, M R Dweck, L Denby and 3 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 39 citations in OpenAlex.

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  13. Tim4 deficiency reduces CD301bInternational journal of oral science · 2024
    Article
  14. Article
  15. Review
  16. Macrophage and T cell networks in adipose tissue.Nature reviews. Endocrinology · 2024
    Review
  17. Review
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 1 country.

M S MagalhaesCentre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.
P SmithCentre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.ORCID http://orcid.org/0000-0001-8986-7361
J R PortmanCentre for Inflammation Research, University of Edinburgh, Edinburgh, UK.
L H Jackson-JonesCentre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.
C C BainCentre for Inflammation Research, University of Edinburgh, Edinburgh, UK.ORCID http://orcid.org/0000-0001-8884-327X
P RamachandranCentre for Inflammation Research, University of Edinburgh, Edinburgh, UK.ORCID http://orcid.org/0000-0001-5996-2413
Z MichailidouCentre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.
R H StimsonCentre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.ORCID http://orcid.org/0000-0002-9002-6188
M R DweckCentre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.
L DenbyCentre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.
N C HendersonCentre for Inflammation Research, University of Edinburgh, Edinburgh, UK.ORCID http://orcid.org/0000-0002-2273-4094
S J JenkinsCentre for Inflammation Research, University of Edinburgh, Edinburgh, UK.ORCID http://orcid.org/0000-0002-0233-5424
C BénézechCentre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK. cbenezec@ed.ac.uk.ORCID http://orcid.org/0000-0002-2613-1418
University of Edinburgh · GBCentre for Inflammation Research · GBLancaster University · GB

Funding

British Heart Foundation FS/14/78/31020Chief Scientist Office SCAF/17/02Medical Research Council MR/L008076/1Medical Research Council MR/M011542/1Medical Research Council MR/N008340/1Wellcome TrustWellcome Trust 219542/Z/19/Z
6 · The paper itself

Abstract

Dyslipidemia is a main driver of cardiovascular diseases. The ability of macrophages to scavenge excess lipids implicate them as mediators in this process and understanding the mechanisms underlying macrophage lipid metabolism is key to the development of new treatments. Here, we investigated how adipose tissue macrophages regulate post-prandial cholesterol transport. Single-cell RNA sequencing and protected bone marrow chimeras demonstrated that ingestion of lipids led to specific transcriptional activation of a population of resident macrophages expressing Lyve1, Tim4, and ABCA1. Blocking the phosphatidylserine receptor Tim4 inhibited lysosomal activation and the release of post-prandial high density lipoprotein cholesterol following a high fat meal. Both effects were recapitulated by chloroquine, an inhibitor of lysosomal function. Moreover, clodronate-mediated cell-depletion implicated Tim4

Indexed as

Adipose TissueAnimalsATP Binding Cassette Transporter 1CholesterolCholesterol, HDLDiet, High-FatLipid MetabolismLysosomesMacrophagesMembrane ProteinsMembrane Transport ProteinsMiceObesityPostprandial PeriodTranscriptional ActivationVesicular Transport ProteinsAbca1 protein, mouseATP Binding Cassette Transporter 1CholesterolCholesterol, HDLLYVE1 protein, mouseMembrane ProteinsMembrane Transport ProteinsTIM-4 protein, mouseVesicular Transport Proteins

Identifiers

PMID34290249
PMCPMC8295389
OpenAlexW3183442433

What OpenQuestion holds

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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.