Evidence map›Paper›PMID 26618077›Full record

ArticleCurrent genetic medicine reports2015

Genetics of non-conventional lipoprotein fractions.

Alexis C Frazier-Wood

Abstract read
In one paragraph

Article in Current genetic medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

1 author.

Alexis C Frazier-WoodUSDA/ARS Children's Nutrition Research Center, Baylor College of Medicine, Houston, Texas USA.

Funding

Genomewide Association Study of Lipid Response to Fenofibrate and Dietary FatR01HL091357 · NHLBI · UNIVERSITY OF KENTUCKY · PI ARNETT, DONNA K · 2008 to 2018
$5.8M
NHLBI NIH HHS R01 HL091357
6 · The paper itself

Abstract

Lipoprotein subclass measures associate with cardiometabolic disease risk. Currently the information that lipoproteins convey on disease risk over that of traditional demographic and lipid measures is minimal, and so their use is clinics is limited. However, lipoprotein subclass perturbations represent some of the earliest manifestations of metabolic dysfunction, and their etiology is partially distinct from lipids, so information on the genetic etiology of lipoproteins offers promise for improved risk prediction, and unique mechanistic insights into IR and atherosclerosis. Here, I review the genetic variants validated as associating with lipoprotein measures to date, and show that the majority of identified variants have functionality that is best understood as related to lipid measures. Until we focus on the genes as they relate to lipoprotein subclass production, we are limiting our understanding of biological mechanisms underlying cardiometabolic disease.

Indexed as

geneticsHDLlipoprotein subfractionsreviewrisk factorssmall LDL

Identifiers

PMID26618077
PMCPMC4658665

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Registered trials

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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.