Evidence map›Paper›PMID 26896185›Full record

ReviewCardiovascular drugs and therapy2016

Human Genetics and the Causal Role of Lipoprotein(a) for Various Diseases.

Florian Kronenberg

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cardiovascular drugs and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

99 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Trial
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Lipoprotein(a): structural basis, bidirectional risk, and therapeutic frontiers.Journal of clinical biochemistry and nutrition · 2026
    Article
  13. Article
  14. Observational
  15. Review
  16. Lipoprotein (a) in primary cardiovascular disease prevention is actionable today.American heart journal plus : cardiology research and practice · 2025
    Review
  17. Review
  18. Article
  19. Review
  20. Article

39 more citing papers are in PubMed but not listed here.

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

1 author.

Florian KronenbergDivision of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University of Innsbruck, Schöpfstr. 41, 6020, Innsbruck, Austria. Florian.Kronenberg@i-med.ac.at.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipoprotein(a) [Lp(a)] is a highly atherogenic lipoprotein that is under strong genetic control by the LPA gene locus. Genetic variants including a highly polymorphic copy number variation of the so called kringle IV repeats at this locus have a pronounced influence on Lp(a) concentrations. High concentrations of Lp(a) as well as genetic variants which are associated with high Lp(a) concentrations are both associated with cardiovascular disease which very strongly supports causality between Lp(a) concetrations and cardiovascular disease. This method of using a genetic variant that has a pronounced influence on a biomarker to support causality with an outcome is called Mendelian randomization approach and was applied for the first time two decades ago with data from Lp(a) and cardiovascular disease. This approach was also used to demonstrate a causal association between high Lp(a) concentrations and aortic valve stenosis, between low concentrations and type-2 diabetes mellitus and to exclude a causal association between Lp(a) concentrations and venous thrombosis. Considering the high frequency of these genetic variants in the population makes Lp(a) the strongest genetic risk factor for cardiovascular disease identified so far. Promising drugs that lower Lp(a) are on the horizon but their efficacy in terms of reducing clinical outcomes still has to be shown.

Indexed as

Cardiovascular DiseasesDNA Copy Number VariationsGenetic MarkersGenetic Predisposition to DiseaseGenetics, MedicalHumansLipoprotein(a)Risk FactorsGenetic MarkersLipoprotein(a)Apolipoprotein(a)Association studyCardiovascular diseaseCopy number variationlipoprotein(a)Mendelian randomization

Identifiers

PMID26896185
PMCPMC4789197

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.