Evidence map›Paper›PMID 35278410›Full record

ArticleJournal of lipid research2022

Apolipoprotein A-V is a potential target for treating coronary artery disease: evidence from genetic and metabolomic analyses.

Dorina Ibi, Manon Boot, Martijn E T Dollé, J Wouter Jukema, Frits R Rosendaal, Constantinos Christodoulides, Matt J Neville, Robert Koivula, Patrick C N Rensen, Fredrik Karpe and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of lipid research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Targeting triglycerides for cardiovascular risk reduction.Internal and emergency medicine · 2026
    Review
  2. Apolipoprotein A (ApoA) in Neurological Disorders: Connections and Insights.International journal of molecular sciences · 2025
    Review
  3. Association ofGenes · 2025
    Observational
  4. Article
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

12 authors at 3 institutions in 2 countries.

Dorina IbiDepartment of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands; Department of Public Health and Primary Care, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands. Electronic address: d.ibi@lumc.nl.
Manon BootDepartment of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands.
Martijn E T DolléDepartment of Public Health and Primary Care, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands.
J Wouter JukemaDepartment of Cardiology, Leiden University Medical Center, Leiden, The Netherlands; Netherlands Heart Institute, Utrecht, The Netherlands.
Frits R RosendaalDepartment of Clinical Epidemiology, Leiden University Medical Center, Leiden, The Netherlands.
Constantinos ChristodoulidesOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Matt J NevilleOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom; NIHR Oxford Biomedical Research Centre, Oxford University Hospitals Foundation Trust, Oxford, United Kingdom.
Robert KoivulaOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Patrick C N RensenDivision of Endocrinology, Department of Internal Medicine, Leiden University Medical Center, Leiden, The Netherlands; Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Fredrik KarpeOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom; NIHR Oxford Biomedical Research Centre, Oxford University Hospitals Foundation Trust, Oxford, United Kingdom.
Raymond NoordamDivision of Gerontology and Geriatrics, Department of Internal Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Ko Willems van DijkDepartment of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands; Division of Endocrinology, Department of Internal Medicine, Leiden University Medical Center, Leiden, The Netherlands; Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Leiden University Medical Center · NLUniversity of Oxford · GBNational Institute for Public Health and the Environment · NL

Funding

British Heart Foundation FS/16/45/32359Medical Research Council MC_PC_17228Medical Research Council MC_QA137853
6 · The paper itself

Abstract

Triglyceride (TG)-lowering LPL variants in combination with genetic LDL-C-lowering variants are associated with reduced risk of coronary artery disease (CAD). Genetic variation in the APOA5 gene encoding apolipoprotein A-V also strongly affects TG levels, but the potential clinical impact and underlying mechanisms are yet to be resolved. Here, we aimed to study the effects of APOA5 genetic variation on CAD risk and plasma lipoproteins through factorial genetic association analyses. Using data from 309,780 European-ancestry participants from the UK Biobank, we evaluated the effects of lower TG levels as a result of genetic variation in APOA5 and/or LPL on CAD risk with or without a background of reduced LDL-C. Next, we compared lower TG levels via APOA5 and LPL variation with over 100 lipoprotein measurements in a combined sample from the Netherlands Epidemiology of Obesity study (N = 4,838) and the Oxford Biobank (N = 6,999). We found that lower TG levels due to combined APOA5 and LPL variation and genetically-influenced lower LDL-C levels afforded the largest reduction in CAD risk (odds ratio: 0.78 (0.73-0.82)). Compared to patients with genetically-influenced lower TG via LPL, genetically-influenced lower TG via APOA5 had similar and independent, but notably larger, effects on the lipoprotein profile. Our results suggest that lower TG levels as a result of APOA5 variation have strong beneficial effects on CAD risk and the lipoprotein profile, which suggest apo A-V may be a potential novel therapeutic target for CAD prevention.

Indexed as

Coronary Artery DiseaseApolipoprotein A-VApolipoproteins ACholesterol, LDLHumansLipoproteinsTriglyceridesAPOA5 protein, humanApolipoprotein A-VApolipoproteins ACholesterol, LDLLipoproteinsTriglyceridescardiovascular diseaseclinical datafactorial analysisgenetic variationhyperlipidemiaLDLlipid-lowering therapylipoprotein lipaselipoproteinstriglycerides

Identifiers

PMID35278410
PMCPMC9062431
OpenAlexW4220837451

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.