Evidence map›Paper›PMID 27460411›Full record

ArticleNature communications2016

ANGPTL4 deficiency in haematopoietic cells promotes monocyte expansion and atherosclerosis progression.

Binod Aryal, Noemi Rotllan, Elisa Araldi, Cristina M Ramírez, Shun He, Benjamin G Chousterman, Ashley M Fenn, Amarylis Wanschel, Julio Madrigal-Matute, Nikhil Warrier and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
7.2field-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

62 citing papers in PubMed, 121 citations in OpenAlex.

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  4. Distinguishing causal from tagging enhancers using single-cell multiome data.medRxiv : the preprint server for health sciences · 2026
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2 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

14 authors at 5 institutions in 2 countries.

Binod AryalVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Noemi RotllanVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Elisa AraldiVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Cristina M RamírezVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Shun HeCenter for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.
Benjamin G ChoustermanCenter for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.
Ashley M FennCenter for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.
Amarylis WanschelDepartments of Medicine and Cell Biology, Leon H. Charney Division of Cardiology and Cell Biology, New York University School of Medicine, New York, New York 10016, USA.
Julio Madrigal-MatuteDepartments of Medicine and Cell Biology, Leon H. Charney Division of Cardiology and Cell Biology, New York University School of Medicine, New York, New York 10016, USA.
Nikhil WarrierDepartments of Medicine and Cell Biology, Leon H. Charney Division of Cardiology and Cell Biology, New York University School of Medicine, New York, New York 10016, USA.
Jose L Martín-VenturaVascular Research Lab, IIS-Fundación Jimenez-Díaz, Universidad Autónoma de Madrid, Madrid 28040, Spain.
Filip K SwirskiCenter for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.
Yajaira SuárezVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Carlos Fernández-HernandoVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Yale University · USNew York University · USCenter for Systems Biology · USMassachusetts General Hospital · USHospital Universitario Fundación Jiménez Díaz · ES

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Yale Pathology Tissue Services Shared ResourceP30CA016359 · NCI · YALE UNIVERSITY · PI DAVID L RIMM · 1985 to 2026
$85.0M
Yale Rheumatic Diseases Research Core CenterP30AR053495 · NIAMS · YALE UNIVERSITY · PI SHLOMCHIK, WARREN D · 2007 to 2017
$7.0M
microRNAs in vascular diseasesR01HL105945 · NHLBI · YALE UNIVERSITY · PI SUAREZ, YAJAIRA · 2011 to 2020
$3.7M
Monocyte Heterogeneity in Experimental and Human AtherosclerosisR01HL095612 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI SWIRSKI, FILIP K · 2009 to 2016
$3.4M
Lifestyle effects on hematopoiesis and atherosclerosisR01HL128264 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NAHRENDORF, MATTHIAS, SWIRSKI, FILIP K · 2015 to 2018
$3.3M
Caveolin-1 in Lipoprotein Metabolism and Atherosclerosis.R01HL106063 · NHLBI · YALE UNIVERSITY · PI FERNANDEZ HERNANDO, CARLOS · 2011 to 2016
$2.5M
Role of microRNAs in lipid metabolism and cardiovascular diseaseR01HL107953 · NHLBI · YALE UNIVERSITY · PI FERNANDEZ HERNANDO, CARLOS · 2011 to 2016
$2.4M
Howard Hughes Medical InstituteNCATS NIH HHS UL1 TR001863NCI NIH HHS P30 CA016359NHLBI NIH HHS R01 HL095612NHLBI NIH HHS R01 HL105945NHLBI NIH HHS R01 HL106063NHLBI NIH HHS R01 HL107953NHLBI NIH HHS R01 HL128264NIAMS NIH HHS P30 AR053495
6 · The paper itself

Abstract

Lipid accumulation in macrophages has profound effects on macrophage gene expression and contributes to the development of atherosclerosis. Here, we report that angiopoietin-like protein 4 (ANGPTL4) is the most highly upregulated gene in foamy macrophages and it's absence in haematopoietic cells results in larger atherosclerotic plaques, characterized by bigger necrotic core areas and increased macrophage apoptosis. Furthermore, hyperlipidemic mice deficient in haematopoietic ANGPTL4 have higher blood leukocyte counts, which is associated with an increase in the common myeloid progenitor (CMP) population. ANGPTL4-deficient CMPs have higher lipid raft content, are more proliferative and less apoptotic compared with the wild-type (WT) CMPs. Finally, we observe that ANGPTL4 deficiency in macrophages promotes foam cell formation by enhancing CD36 expression and reducing ABCA1 localization in the cell surface. Altogether, these findings demonstrate that haematopoietic ANGPTL4 deficiency increases atherogenesis through regulating myeloid progenitor cell expansion and differentiation, foam cell formation and vascular inflammation.

Indexed as

Disease ProgressionAngiopoietin-Like Protein 4AnimalsApoptosisAtherosclerosisBone Marrow TransplantationCell ProliferationCell SurvivalFoam CellsHematopoietic Stem CellsHumansInflammationLeukocytosisMacrophagesMaleMiceAngiopoietin-Like Protein 4

Identifiers

PMID27460411
PMCPMC4974469
OpenAlexW2481843462

What OpenQuestion holds

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LicenceCC BY
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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.