Evidence map›Paper›PMID 25964513›Full record

ArticleJournal of lipid research2015

Increased plasma cholesterol esterification by LCAT reduces diet-induced atherosclerosis in SR-BI knockout mice.

Seth G Thacker, Xavier Rousset, Safiya Esmail, Abdalrahman Zarzour, Xueting Jin, Heidi L Collins, Maureen Sampson, John Stonik, Stephen Demosky, Daniela A Malide and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 53 citations in OpenAlex.

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  10. High Free Cholesterol Bioavailability Drives the Tissue Pathologies in Scarb1Arteriosclerosis, thrombosis, and vascular biology · 2021
    Article
  11. Review
  12. Good Cholesterol Gone Bad? HDL and COVID-19.International journal of molecular sciences · 2021
    Review
  13. Article
  14. Article
  15. Nutrients · 2020
    Article
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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

15 authors at 3 institutions in 1 country.

Seth G ThackerLipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Xavier RoussetLipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Safiya EsmailLipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Abdalrahman ZarzourLipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Xueting JinExperimental Atherosclerosis Section, Center for Molecular, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Heidi L CollinsVascular Strategies LLC, Plymouth Meeting, PA 19462.
Maureen SampsonDepartment of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, MD 20892.
John StonikLipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Stephen DemoskyLipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Daniela A MalideLight Microscopy Core, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Lita FreemanLipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Boris L VaismanLipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Howard S KruthExperimental Atherosclerosis Section, Center for Molecular, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Steven J AdelmanVascular Strategies LLC, Plymouth Meeting, PA 19462.
Alan T RemaleyLipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
National Heart Lung and Blood Institute · USNational Institutes of Health · USNational Institutes of Health Clinical Center · US

Funding

NHLBI Animal Program DivisionZIGHL006020 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI CLARK, TANNIA · 2009 to 2025
$47.3M
Light Microscopy CoreZICHL006019 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI COMBS, CHRISTIAN · 2009 to 2025
$29.3M
Use Of Animal Models To Study Lipid Genes That Modulate AtherosclerosisZIAHL002058 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI REMALEY, ALAN THOMAS · 2009 to 2019
$14.3M
Development of recombinant Lecithin Cholesterol Acyltransferase as a therapeuticZIAHL006092 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI REMALEY, ALAN THOMAS · 2010 to 2021
$13.0M
Intramural NIH HHS
6 · The paper itself

Abstract

LCAT, a plasma enzyme that esterifies cholesterol, has been proposed to play an antiatherogenic role, but animal and epidemiologic studies have yielded conflicting results. To gain insight into LCAT and the role of free cholesterol (FC) in atherosclerosis, we examined the effect of LCAT over- and underexpression in diet-induced atherosclerosis in scavenger receptor class B member I-deficient [Scarab(-/-)] mice, which have a secondary defect in cholesterol esterification. Scarab(-/-)×LCAT-null [Lcat(-/-)] mice had a decrease in HDL-cholesterol and a high plasma ratio of FC/total cholesterol (TC) (0.88 ± 0.033) and a marked increase in VLDL-cholesterol (VLDL-C) on a high-fat diet. Scarab(-/-)×LCAT-transgenic (Tg) mice had lower levels of VLDL-C and a normal plasma FC/TC ratio (0.28 ± 0.005). Plasma from Scarab(-/-)×LCAT-Tg mice also showed an increase in cholesterol esterification during in vitro cholesterol efflux, but increased esterification did not appear to affect the overall rate of cholesterol efflux or hepatic uptake of cholesterol. Scarab(-/-)×LCAT-Tg mice also displayed a 51% decrease in aortic sinus atherosclerosis compared with Scarab(-/-) mice (P < 0.05). In summary, we demonstrate that increased cholesterol esterification by LCAT is atheroprotective, most likely through its ability to increase HDL levels and decrease pro-atherogenic apoB-containing lipoprotein particles.

Indexed as

AnimalsAtherosclerosisBiological TransportBlood PlateletsCD36 AntigensCholesterolDiet, High-FatErythrocyte CountErythrocytesEsterificationFemaleGene Expression Regulation, EnzymologicGene Knockout TechniquesHumansLipoproteins, VLDLLiverCD36 AntigensCholesterolLipoproteins, VLDLPhosphatidylcholine-Sterol O-Acyltransferaseknockoutlecithin:cholesterol acyltransferasescavenger receptor class B member I

Identifiers

PMID25964513
PMCPMC4479333
OpenAlexW2160840655

What OpenQuestion holds

Textmetadata
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.