Evidence map›Paper›PMID 28534127›Full record

ReviewCurrent atherosclerosis reports2017

Genetics of Triglycerides and the Risk of Atherosclerosis.

Jacqueline S Dron, Robert A Hegele

Open access · hybridAbstract readReview
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 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
10.2field-weighted citation impact, top 1% 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

50 citing papers in PubMed, 107 citations in OpenAlex.

  1. Trial
  2. Effects ofNutrients · 2020
    Trial
  3. Article
  4. Article
  5. Review
  6. Article
  7. Association ofGenes · 2025
    Observational
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Editorial: Highlights in Lipids in Cardiovascular Disease: 2021.Frontiers in cardiovascular medicine · 2022
    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

2 authors at 1 institution in 1 country.

Jacqueline S DronDepartment of Biochemistry, Schulich School of Medicine and Dentistry, Western University, London, ON, Canada.
Robert A HegeleDepartment of Biochemistry, Schulich School of Medicine and Dentistry, Western University, London, ON, Canada. hegele@robarts.ca.
Western University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewPlasma triglycerides are routinely measured with a lipid profile, and elevated plasma triglycerides are commonly encountered in the clinic. The confounded nature of this trait, which is correlated with numerous other metabolic perturbations, including depressed high-density lipoprotein cholesterol (HDL-C), has thwarted efforts to directly implicate triglycerides as causal in atherogenesis. Human genetic approaches involving large-scale populations and high-throughput genomic assessment under a Mendelian randomization framework have undertaken to sort out questions of causality. RECENT

findingsWe review recent large-scale meta-analyses of cohorts and population-based sequencing studies designed to address whether common and rare variants in genes whose products are determinants of plasma triglycerides are also associated with clinical cardiovascular endpoints. The studied loci include genes encoding lipoprotein lipase and proteins that interact with it, such as apolipoprotein (apo) A-V, apo C-III and angiopoietin-like proteins 3 and 4, and common polymorphisms identified in genome-wide association studies. Triglyceride-raising variant alleles of these genes showed generally strong associations with clinical cardiovascular endpoints. However, in most cases, a second lipid disturbance-usually depressed HDL-C-was concurrently associated. While the findings collectively shift our understanding towards a potential causal role for triglycerides, we still cannot rule out the possibilities that triglycerides are a component of a joint phenotype with low HDL-C or that they are but markers of deeper causal metabolic disturbances that are not routinely measured in epidemiological-scale genetic studies.

Indexed as

AtherosclerosisHypertriglyceridemiaTriglyceridesCholesterol, HDLGenome-Wide Association StudyHumansPolymorphism, GeneticCholesterol, HDLTriglyceridesComplex traitDNA sequencingGenetic associationMendelian randomizationMonogenicPolygenic

Identifiers

PMID28534127
PMCPMC5440481
OpenAlexW2617842398

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.