Evidence map›Paper›PMID 18415697›Full record

ReviewJournal of inherited metabolic disease2008

Apoprotein A-V: an important regulator of triglyceride metabolism.

M Kluger, J Heeren, M Merkel

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of inherited metabolic disease, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 47 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Association ofFrontiers in genetics · 2025
    Article
  5. Polygenic Risk of Hypertriglyceridemia Is Modified by BMI.International journal of molecular sciences · 2022
    Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Clinofibrate improved canine lipid metabolism in some but not all breeds.The Journal of veterinary medical science · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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 at 2 institutions in 1 country.

M KlugerIII Department of Internal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
J Heeren
M Merkel
Universität Hamburg · DEAsklepios Klinik St. Georg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apolipoprotein A-V (apoA-V) was discovered in 2001 both by comparative sequencing and as a liver regeneration protein. The gene is a located at the APOA1/C3/A4/A5 gene cluster on chromosome 11q23, a locus well known for playing a major role in regulating plasma cholesterol and triglyceride (TG) levels. ApoA-V is produced in the liver and has very low plasma concentrations (0.1-0.4 mug/ml). Mice lacking apoA-V have 4-fold increased TG levels, whereas apoA-V overexpression leads to 40% plasma TG reduction. Based on metabolic studies in vivo, apoA-V enhances the catabolism of TG rich lipoproteins rather than affecting their intestinal or hepatic production. By activating proteoglycans-bound lipoprotein lipase (LPL), apoA-V can accelerate TG hydrolysis from VLDL and chylomicrons independent from other apoproteins. Several variants at the APOA5 gene locus have been detected in humans. Some single nucleotide polymorphisms (SNPs) are associated with significantly higher plasma TG levels in patients (e.g., -1131T > C, S19W, G185C). In addition, these SNPs may affect fibrate response and obesity. However, data for a possible association of APOA5 variants with coronary heart disease are not consistent. Severe structural mutations (Q139X, Q148X, IVS3 + 3G > C) predispose to familial hypertriglyceridaemia and late-onset chylomicronaemia. Thus, despite its low plasma concentration, apoA-V is a major regulator of plasma TG metabolism in humans. However, the precise mechanism of its function is not yet clear.

Indexed as

AnimalsApolipoprotein A-VApolipoproteinsApolipoproteins ADisease Models, AnimalGenetic Predisposition to DiseaseHumansLipid Metabolism, Inborn ErrorsLipolysisLiverMiceMutationPhenotypeTriglyceridesAPOA5 protein, humanApoa5 protein, mouseApolipoprotein A-VApolipoproteinsApolipoproteins ATriglycerides

Identifiers

PMID18415697
OpenAlexW1991208787

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.