Evidence map›Paper›PMID 32099678›Full record

ReviewJournal of lipids2020

Lipoprotein(a) the Insurgent: A New Insight into the Structure, Function, Metabolism, Pathogenicity, and Medications Affecting Lipoprotein(a) Molecule.

Motasim M Jawi, Jiri Frohlich, Sammy Y Chan

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of lipids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 3 pooled it
11.6field-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

63 citing papers in PubMed, 3 syntheses or guidelines pooled it, 171 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Lipoprotein(a) Does Not Correlate with Hypertensive Mediated Organ Damage and Subsequent Cardiovascular Events in a Primary Prevention Cohort.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2026
    Article
  7. Article
  8. Article
  9. The Emerging Lipid Risk: Lipoprotein(a).Korean circulation journal · 2026
    Review
  10. Article
  11. Review
  12. Review
  13. Lipoprotein(a): structural basis, bidirectional risk, and therapeutic frontiers.Journal of clinical biochemistry and nutrition · 2026
    Article
  14. Observational
  15. Article
  16. Article
  17. Article
  18. Article
  19. Advances in laboratory medicine · 2025
    Article
  20. Novel Circulating Biomarkers in Aortic Valve Stenosis.International journal of molecular sciences · 2025
    Review

3 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

3 authors at 1 institution in 2 countries.

Motasim M JawiHealthy Heart Program, St. Paul's Hospital, Vancouver V6Z 1Y6, Canada.ORCID https://orcid.org/0000-0002-2559-9019
Jiri FrohlichHealthy Heart Program, St. Paul's Hospital, Vancouver V6Z 1Y6, Canada.
Sammy Y ChanHealthy Heart Program, St. Paul's Hospital, Vancouver V6Z 1Y6, Canada.
University of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipoprotein(a) [Lp(a)], aka "Lp little a", was discovered in the 1960s in the lab of the Norwegian physician Kåre Berg. Since then, we have greatly improved our knowledge of lipids and cardiovascular disease (CVD). Lp(a) is an enigmatic class of lipoprotein that is exclusively formed in the liver and comprises two main components, a single copy of apolipoprotein (apo) B-100 (apo-B100) tethered to a single copy of a protein denoted as apolipoprotein(a) apo(a). Plasma levels of Lp(a) increase soon after birth to a steady concentration within a few months of life. In adults, Lp(a) levels range widely from <2 to 2500 mg/L. Evidence that elevated Lp(a) levels >300 mg/L contribute to CVD is significant. The improvement of isoform-independent assays, together with the insight from epidemiologic studies, meta-analyses, genome-wide association studies, and Mendelian randomization studies, has established Lp(a) as the single most common independent genetically inherited causal risk factor for CVD. This breakthrough elevated Lp(a) from a biomarker of atherosclerotic risk to a target of therapy. With the emergence of promising second-generation antisense therapy, we hope that we can answer the question of whether Lp(a) is ready for prime-time clinic use. In this review, we present an update on the metabolism, pathophysiology, and current/future medical interventions for high levels of Lp(a).

Identifiers

PMID32099678
PMCPMC7016456
OpenAlexW3003956143

What Socratic 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 Socratic graph.