Evidence map›Paper›PMID 28500476›Full record

ReviewCurrent atherosclerosis reports2017

Update on APOA5 Genetics: Toward a Better Understanding of Its Physiological Impact.

Montse Guardiola, Josep Ribalta

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current atherosclerosis reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 3 pooled it
2.4field-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

35 citing papers in PubMed, 3 syntheses or guidelines pooled it, 62 citations in OpenAlex.

  1. Pooled it
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  4. Trial
  5. Review
  6. Article
  7. Familial Combined Hyperlipidemia: Myth or Reality?Current atherosclerosis reports · 2025
    Review
  8. Article
  9. Association ofFrontiers in genetics · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. A unified model for regulating lipoprotein lipase activity.Trends in endocrinology and metabolism: TEM · 2024
    Review
  14. Review
  15. [A case of sudden hearing loss combined with familial hyperlipidemia].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2024
    Article
  16. Review
  17. Article
  18. Review
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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

2 authors at 2 institutions in 1 country.

Montse GuardiolaUnitat de Recerca en Lípids i Arteriosclerosi, Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, Institut d'Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, Sant Llorenç 21, 43201, Reus, Spain.
Josep RibaltaUnitat de Recerca en Lípids i Arteriosclerosi, Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, Institut d'Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, Sant Llorenç 21, 43201, Reus, Spain. josep.ribalta@urv.cat.
Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ESInstitut d'Investigació Sanitària Pere Virgili · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewThis review is intended to summarize the genetic studies published during the last 3 years that help us understand the physiology of apoAV and its clinical implications. RECENT

findingsAPOA5 is probably the gene with the strongest effect on triglyceride (TG) metabolism. APOA5 is almost exclusively expressed in the liver, and its product apoAV has a very low circulating concentration. New physiological roles of apoAV have been recently elucidated, such as control of chylomicron production in the intestine and TG accumulation in adipose tissue. The key role of APOA5 in TG metabolism has been largely shown through genetic studies in association with either severe or moderate hypertriglyceridemia. Studies suggest that APOA5 variants affect not only total TG concentrations but also the entire lipoprotein subclass distribution, shifting them toward atherogenic dyslipidemia in high-risk subjects. Environmental interactions and epigenetic factors are also crucial in regulating these processes. Delineation of the mechanisms involved in the transcriptional control of the gene, combined with determination of biological significance of the SNPs in the APOA5 locus, would help to fully understand the effect of APOA5 on TGs. In summary, APOA5 variants cause hypertriglyceridemia. In high cardiovascular risk patients (e.g., patients with metabolic syndrome or type 2 diabetes), APOA5 variants elevate TG levels and shift the entire lipoprotein subclass distribution toward atherogenic dyslipidemia. At a physiological level, apoAV seems to encompass more roles than those initially suggested after its discovery.

Indexed as

HypertriglyceridemiaApolipoprotein A-VAtherosclerosisHumansPolymorphism, Single NucleotideTriglyceridesAPOA5 protein, humanApolipoprotein A-VTriglyceridesAPOA5EpigeneticPolymorphismTriglycerides

Identifiers

PMID28500476
OpenAlexW2613642286

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.