Evidence map›Paper›PMID 25341944›Full record

ArticleJournal of lipid research2014

Defective functionality of HDL particles in familial apoA-I deficiency: relevance of alterations in HDL lipidome and proteome.

Fabiana Rached, Raul D Santos, Laurent Camont, Marcio H Miname, Marie Lhomme, Carolane Dauteuille, Sora Lecocq, Carlos V Serrano, M John Chapman, Anatol Kontush

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 36 citations in OpenAlex.

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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

10 authors at 3 institutions in 3 countries.

Fabiana RachedNational Institute for Health and Medical Research (INSERM), UMR-ICAN 1166, University of Pierre and Marie Curie - Paris 6, Pitié - Salpétrière University Hospital, ICAN, Paris, France Heart Institute-InCor, University of Sao Paulo, Sao Paulo, Brazil.
Raul D SantosHeart Institute-InCor, University of Sao Paulo, Sao Paulo, Brazil.
Laurent CamontNational Institute for Health and Medical Research (INSERM), UMR-ICAN 1166, University of Pierre and Marie Curie - Paris 6, Pitié - Salpétrière University Hospital, ICAN, Paris, France.
Marcio H MinameHeart Institute-InCor, University of Sao Paulo, Sao Paulo, Brazil.
Marie LhommeNational Institute for Health and Medical Research (INSERM), UMR-ICAN 1166, University of Pierre and Marie Curie - Paris 6, Pitié - Salpétrière University Hospital, ICAN, Paris, France.
Carolane DauteuilleNational Institute for Health and Medical Research (INSERM), UMR-ICAN 1166, University of Pierre and Marie Curie - Paris 6, Pitié - Salpétrière University Hospital, ICAN, Paris, France.
Sora LecocqNational Institute for Health and Medical Research (INSERM), UMR-ICAN 1166, University of Pierre and Marie Curie - Paris 6, Pitié - Salpétrière University Hospital, ICAN, Paris, France.
Carlos V SerranoHeart Institute-InCor, University of Sao Paulo, Sao Paulo, Brazil.
M John ChapmanNational Institute for Health and Medical Research (INSERM), UMR-ICAN 1166, University of Pierre and Marie Curie - Paris 6, Pitié - Salpétrière University Hospital, ICAN, Paris, France.
Anatol KontushNational Institute for Health and Medical Research (INSERM), UMR-ICAN 1166, University of Pierre and Marie Curie - Paris 6, Pitié - Salpétrière University Hospital, ICAN, Paris, France.
National Institutes of Health · USUniversidade de São Paulo · BRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To evaluate functional and compositional properties of HDL in subjects from a kindred of genetic apoA-I deficiency, two homozygotes and six heterozygotes, with a nonsense mutation at APOA1 codon -2, Q[-2]X, were recruited together with age- and sex-matched healthy controls (n = 11). Homozygotes displayed undetectable plasma levels of apoA-I and reduced levels of HDL-cholesterol (HDL-C) and apoC-III (5.4% and 42.6% of controls, respectively). Heterozygotes displayed low HDL-C (21 ± 9 mg/dl), low apoA-I (79 ± 24 mg/dl), normal LDL-cholesterol (132 ± 25 mg/dl), and elevated TG (130 ± 45 mg/dl) levels. Cholesterol efflux capacity of ultracentrifugally isolated HDL subpopulations was reduced (up to -25%, P < 0.01, on a glycerophospholipid [GP] basis) in heterozygotes versus controls. Small, dense HDL3 and total HDL from heterozygotes exhibited diminished antioxidative activity (up to -48%, P < 0.001 on a total mass basis) versus controls. HDL subpopulations from both homozygotes and heterozygotes displayed altered chemical composition, with depletion in apoA-I, GP, and cholesteryl ester; enrichment in apoA-II, free cholesterol, and TG; and altered phosphosphingolipidome. The defective atheroprotective activities of HDL were correlated with altered lipid and apo composition. These data reveal that atheroprotective activities of HDL particles are impaired in homozygous and heterozygous apoA-I deficiency and are intimately related to marked alterations in protein and lipid composition.

Indexed as

AdultApolipoprotein A-IApolipoprotein C-IIIBrazilCholesterol EstersCholesterol Ester Transfer ProteinsCholesterol, HDLCholesterol, LDLCodon, NonsenseFamily HealthFemaleHeterozygoteHomozygoteHumansHypoalphalipoproteinemiasLipoproteins, HDLAPOA1 protein, humanApolipoprotein A-IApolipoprotein C-IIICETP protein, humanCholesterol EstersCholesterol Ester Transfer ProteinsCholesterol, HDLCholesterol, LDLCodon, NonsenseLipoproteins, HDLLipoproteins, HDL3PhospholipidsSphingolipidsTriglyceridesantioxidative activityapolipoprotein A-Icellular cholesterol effluxfamilial deficiencygeneticsHDL functionalityhigh density lipoproteinlipidomics

Identifiers

PMID25341944
PMCPMC4242444
OpenAlexW2007776103

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.