Evidence map›Paper›PMID 26647358›Full record

ReviewJournal of lipid research2016

Lipoprotein (a): truly a direct prothrombotic factor in cardiovascular disease?

Michael B Boffa, Marlys L Koschinsky

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of lipid research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
143citing papers in PubMed, 2 pooled it
10.0field-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

143 citing papers in PubMed, 2 syntheses or guidelines pooled it, 285 citations in OpenAlex.

  1. Pooled it
  2. Guideline
  3. Trial
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  9. Review
  10. Lipoprotein(a) and premature myocardial infarction: Mechanistic insights and implications for PCI-era residual risk.International journal of cardiology. Cardiovascular risk and prevention · 2026
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. The Emerging Lipid Risk: Lipoprotein(a).Korean circulation journal · 2026
    Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article

83 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

2 authors at 2 institutions in 1 country.

Michael B BoffaDepartment of Chemistry and Biochemistry, University of Windsor, Windsor, ON, Canada.
Marlys L KoschinskyDepartment of Chemistry and Biochemistry, University of Windsor, Windsor, ON, Canada Robarts Research Institute, Western University, London, ON, Canada mlk@robarts.ca.
University of Windsor · CAWestern University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elevated plasma concentrations of lipoprotein (a) [Lp(a)] have been determined to be a causal risk factor for coronary heart disease, and may similarly play a role in other atherothrombotic disorders. Lp(a) consists of a lipoprotein moiety indistinguishable from LDL, as well as the plasminogen-related glycoprotein, apo(a). Therefore, the pathogenic role for Lp(a) has traditionally been considered to reflect a dual function of its similarity to LDL, causing atherosclerosis, and its similarity to plasminogen, causing thrombosis through inhibition of fibrinolysis. This postulate remains highly speculative, however, because it has been difficult to separate the prothrombotic/antifibrinolytic functions of Lp(a) from its proatherosclerotic functions. This review surveys the current landscape surrounding these issues: the biochemical basis for procoagulant and antifibrinolytic effects of Lp(a) is summarized and the evidence addressing the role of Lp(a) in both arterial and venous thrombosis is discussed. While elevated Lp(a) appears to be primarily predisposing to thrombotic events in the arterial tree, the fact that most of these are precipitated by underlying atherosclerosis continues to confound our understanding of the true pathogenic roles of Lp(a) and, therefore, the most appropriate therapeutic target through which to mitigate the harmful effects of this lipoprotein.

Indexed as

AnimalsCardiovascular DiseasesHumansHyperlipidemiasLipoprotein(a)PlasminogenStructural Homology, ProteinThrombosisLipoprotein(a)Plasminogenapolipoprotein (a)apolipoproteinsatherosclerosiscoagulationfibrinolysislipoproteinslipoproteins/kineticslow density lipoproteinthrombosis

Identifiers

PMID26647358
PMCPMC4847635
OpenAlexW2234206893

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.