Evidence map›Paper›PMID 25995210›Full record

ArticleJournal of lipid research2015

Inflammatory remodeling of the HDL proteome impairs cholesterol efflux capacity.

Tomáš Vaisar, Chongren Tang, Ilona Babenko, Patrick Hutchins, Jake Wimberger, Anthony F Suffredini, Jay W Heinecke

Abstract 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 122 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

122 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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62 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Tomáš VaisarDepartment of Medicine, University of Washington, Seattle, WA 98105.
Chongren TangDepartment of Medicine, University of Washington, Seattle, WA 98105.
Ilona BabenkoDepartment of Medicine, University of Washington, Seattle, WA 98105.
Patrick HutchinsDepartment of Medicine, University of Washington, Seattle, WA 98105.
Jake WimbergerDepartment of Medicine, University of Washington, Seattle, WA 98105.
Anthony F SuffrediniCritical Care Medicine Department, National Institutes of Health, Bethesda, MD 20892.
Jay W HeineckeDepartment of Medicine, University of Washington, Seattle, WA 98105.

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Sakeneh Zraika · 1986 to 2026
$41.4M
PILOT STUDY--CLINICAL NUTRITION RESEARCHP30DK035816 · NIDDK · UNIVERSITY OF WASHINGTON · PI Ellen A Schur · 1986 to 2026
$30.4M
Role of Serum Amyloid A in Diabetic Vascular DiseaseP01HL092969 · NHLBI · UNIVERSITY OF WASHINGTON · PI BORNFELDT, KARIN E. · 2008 to 2019
$23.5M
REVERSE CHOLESTEROL TRANSPORT IN DIABETESP01DK002456 · NIDDK · UNIVERSITY OF WASHINGTON · PI CHAIT, ALAN · 1986 to 2007
$10.2M
Plaque Inflammation and Dysfunctional HDL in AIM-HIGHR01HL089504 · NHLBI · UNIVERSITY OF WASHINGTON · PI O'BRIEN, KEVIN D. · 2008 to 2012
$2.2M
Quantitative Assessment of HDL FunctionR01HL112625 · NHLBI · UNIVERSITY OF WASHINGTON · PI HEINECKE, JAY W · 2012 to 2016
$2.1M
Molecular Mechanisms for Dysfunctional High Density Lipoprotein (HDL)R01HL086798 · NHLBI · UNIVERSITY OF WASHINGTON · PI HEINECKE, JAY W · 2007 to 2011
$1.9M
Cardioprotective Mechanisms of HDLR01HL108897 · NHLBI · UNIVERSITY OF WASHINGTON · PI HEINECKE, JAY W · 2012 to 2015
$1.7M
NHLBI NIH HHS HL086798NHLBI NIH HHS HL089504NHLBI NIH HHS HL108897NHLBI NIH HHS HL112625NHLBI NIH HHS P01 HL092969NHLBI NIH HHS R01 HL086798NHLBI NIH HHS R01 HL089504NHLBI NIH HHS R01 HL108897NHLBI NIH HHS R01 HL112625NIDDK NIH HHS DK002456NIDDK NIH HHS DK035816NIDDK NIH HHS P01 DK002456NIDDK NIH HHS P30 DK017047NIDDK NIH HHS P30 DK035816
6 · The paper itself

Abstract

Recent studies demonstrate that HDL's ability to promote cholesterol efflux from macrophages associates strongly with cardioprotection in humans independently of HDL-cholesterol (HDL-C) and apoA-I, HDL's major protein. However, the mechanisms that impair cholesterol efflux capacity during vascular disease are unclear. Inflammation, a well-established risk factor for cardiovascular disease, has been shown to impair HDL's cholesterol efflux capacity. We therefore tested the hypothesis that HDL's impaired efflux capacity is mediated by specific changes of its protein cargo. Humans with acute inflammation induced by low-level endotoxin had unchanged HDL-C levels, but their HDL-C efflux capacity was significantly impaired. Proteomic analyses demonstrated that HDL's cholesterol efflux capacity correlated inversely with HDL content of serum amyloid A (SAA)1 and SAA2. In mice, acute inflammation caused a marked impairment of HDL-C efflux capacity that correlated with a large increase in HDL SAA. In striking contrast, the efflux capacity of mouse inflammatory HDL was preserved with genetic ablation of SAA1 and SAA2. Our observations indicate that the inflammatory impairment of HDL-C efflux capacity is due in part to SAA-mediated remodeling of HDL's protein cargo.

Indexed as

AdultAnimalsCholesterol, HDLCytoprotectionEndotoxinsHumansInflammationMacrophagesMaleMiceMyocardiumProteomeSerum Amyloid A ProteinCholesterol, HDLEndotoxinsProteomeSerum Amyloid A Proteinapolipoproteinsatherosclerosishigh density lipoproteininflammationmass spectrometryproteomics

Identifiers

PMID25995210
PMCPMC4513993

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.