Evidence map›Paper›PMID 26028042›Full record

ReviewCurrent drug targets2015

Apolipoprotein A5: Extracellular and Intracellular Roles in Triglyceride Metabolism.

Trudy M Forte, Robert O Ryan

Open access · greenAbstract readReview
In one paragraph

Review in Current drug targets, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Article
  3. Biomedicines · 2024
    Review
  4. Nomogram developed withCardiovascular diagnosis and therapy · 2024
    Article
  5. Review
  6. Review
  7. Article
  8. Olanzapine causes non-alcoholic fatty liver disease via inhibiting the secretion of apolipoprotein A5.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  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

2 authors at 1 institution in 1 country.

Trudy M ForteCenter for Prevention of Obesity, Diabetes and Cardiovascular Disease, Children`s Hospital Oakland Research Institute, Oakland, CA 94609, USA. tforte@chori.org.
Robert O Ryan
California Department of Public Health · US

Funding

Effect of Apolipoprotein Structural AdaptabilityR37HL064159 · NHLBI · UNIVERSITY OF NEVADA RENO · PI RYAN, ROBERT O'MARA · 2010 to 2019
$4.1M
EFFECT OF APOLIPOPROTEIN STRUCTURAL ADAPTABILITYR01HL064159 · NHLBI · CHILDREN'S HOSPITAL &RES CTR AT OAKLAND · PI RYAN, ROBERT O'MARA · 2000 to 2009
$3.6M
Apolipoprotein A-V: A Functional Proteomics StudyR01HL073061 · NHLBI · CHILDREN'S HOSPITAL &RES CTR AT OAKLAND · PI RYAN, ROBERT O'MARA · 2004 to 2010
$2.4M
NHLBI NIH HHS HL-073061NHLBI NIH HHS HL-64159NHLBI NIH HHS R01 HL064159NHLBI NIH HHS R01 HL073061NHLBI NIH HHS R37 HL064159
6 · The paper itself

Abstract

This review addresses two major functions of apolipoprotein (apo) A5 including (1) its role in maintaining normal plasma levels of circulating triglyceride (TG) and (2) its role as a component of hepatic lipid droplets. ApoA5 is synthesized solely in the liver and circulating concentrations are extremely low. In the plasma, ApoA5 associates with TG-rich lipoproteins and enhances TG hydrolysis and remnant lipoprotein clearance. ApoA5 loss-of-function single nucleotide polymorphisms are associated with reduced lipolysis, poor remnant clearance and concomitantly, hypertriglyceridemia. Although there have been substantial breakthroughs in understanding pathophysiology associated with secreted ApoA5, there is a paucity of knowledge on the functionality of intracellular ApoA5. However, recent studies indicate that overexpression of intracellular ApoA5 is positively associated with accumulation of TG-rich lipid droplets in hepatocytes. It is thought that ApoA5 may have a causal role in non-alcoholic fatty liver disease (NAFLD) and thus, may serve as a target for developing therapeutics for NAFLD.

Indexed as

Apolipoprotein A-VApolipoproteins AHumansHypertriglyceridemiaLiverNon-alcoholic Fatty Liver DiseasePolymorphism, Single NucleotideTriglyceridesAPOA5 protein, humanApolipoprotein A-VApolipoproteins ATriglycerides

Identifiers

PMID26028042
PMCPMC6594035
OpenAlexW2410968861

What OpenQuestion holds

Textmetadata
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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.