Evidence map›Paper›PMID 17969379›Full record

ReviewVascular health and risk management2007

Apolipoproteins A-I and B: biosynthesis, role in the development of atherosclerosis and targets for intervention against cardiovascular disease.

Sven-Olof Olofsson, Olov Wiklund, Jan Borén

Open access · greenAbstract readReview
In one paragraph

Review in Vascular health and risk management, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 68 citations in OpenAlex.

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  18. Atherogenic dyslipidemia.Indian journal of endocrinology and metabolism · 2013
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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

3 authors.

Sven-Olof OlofssonSahlgrenska Center for Cardiovascular and Metabolic Research, the Wallenberg Laboratory University of Göteborg, Sweden. Sven-Olof.Olofsson@wlab.gu.se
Olov Wiklund
Jan Borén

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apolipoprotein (apo) AI and apoB are the major apolipoproteins of high-density lipoprotein (HDL) and low-density lipoprotein (LDL), respectively. ApoB assembles the precursor of LDL, very-low-density lipoprotein (VLDL), in the liver. The assembly starts with the formation of a primordial particle, which is converted to VLDL2. The VLDL2 particle is then transferred to the Golgi apparatus and can either be secreted or converted to triglyceride-rich VLDL1. We have reviewed this assembly process, the process involved in the storage of triglycerides in cytosolic lipid droplets, and the relationship between these two processes. We also briefly discuss the formation ofHDL. ApoB mediates the interaction between LDL and the arterial wall. Two regions in apoB are involved in this binding. This interaction and its role in the development of atherosclerosis are reviewed. ApoB can be used to measure the number of LDL or VLDL particles present in plasma, as there is one molecule of apoB on each particle. By contrast, the amount of cholesterol and other lipids on each particle varies under different conditions. We address the possibility of using apoAl and apoB levels to estimate the risk of development of cardiovascular diseases and to monitor intervention to treat these diseases.

Indexed as

AnimalsApolipoprotein A-IApolipoprotein B-100AtherosclerosisBiomarkersCardiovascular DiseasesCholesterol, HDLFemaleGolgi ApparatusHumansLipoproteins, VLDLMiceApolipoprotein A-IApolipoprotein B-100BiomarkersCholesterol, HDLLipoproteins, VLDL

Identifiers

PMID17969379
PMCPMC2291326
OpenAlexW139484856

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.