Evidence map›Paper›PMID 23040268›Full record

ReviewMetabolism: clinical and experimental2013

Lipoprotein(a) metabolism: potential sites for therapeutic targets.

Jane Hoover-Plow, Menggui Huang

Registry-linked trialOpen access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Metabolism: clinical and experimental, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04993664 (Influence of Pelacarsen on Arterial Wall Properties and Risk Factors in Patients After Myocardial Infarction With High Lp), which is not on this map. Cited by 68 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 4 pooled it
10.9field-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.

NCT04993664 nawithdrawnnot on this mapstarted 2021, after this paper: background citation

Influence of Pelacarsen on Arterial Wall Properties and Risk Factors in Patients After Myocardial Infarction With High Lp(a) Values

TypeinterventionalSponsorUniversity Medical Centre LjubljanaRan2021 to 2022Enrolled0ConditionsAcute Coronary Syndrome, Lipoproteinemia, Inflammation, Genetic PolymorphismsArmsPelacarsen (TQJ230), Placebo
3 · Its place in the literature

Who cites it

68 citing papers in PubMed, 4 syntheses or guidelines pooled it, 171 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Trial
  7. Trial
  8. Review
  9. Review
  10. Article
  11. Lipoprotein(a) and cardiovascular disease.The Biochemical journal · 2024
    Review
  12. Article
  13. Article
  14. Review
  15. Lipoprotein(a): Just an Innocent Bystander in Arterial Hypertension?International journal of molecular sciences · 2023
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

8 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.

Jane Hoover-PlowJ. J. Jacobs Center for Thrombosis and Vascular Biology, Department of Cardiovascular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44139, USA. hooverj@ccf.org
Menggui Huang
Cleveland Clinic Lerner College of Medicine · USJacobs (United States) · US

Funding

Regulation of Leukocyte Migration by PlasminogenR01HL078701 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI HOOVER-PLOW, JANE LEE · 2004 to 2013
$2.7M
SYSTEMATIC EVALUATION OF THE PLASMINOGEN SYSTEM IN MICER01HL065204 · NHLBI · CLEVELAND CLINIC FOUNDATION · PI HOOVER-PLOW, JANE LEE · 2000 to 2003
$1.2M
NHLBI NIH HHS HL078701NHLBI NIH HHS R01 HL065204NHLBI NIH HHS R01 HL078701
6 · The paper itself

Abstract

Lipoprotein(a) [Lp(a)] resembles low-density lipoprotein (LDL), with an LDL lipid core and apolipoprotein B (apoB), but contains a unique apolipoprotein, apo(a). Elevated Lp(a) is an independent risk factor for coronary and peripheral vascular diseases. The size and concentration of plasma Lp(a) are related to the synthetic rate, not the catabolic rate, and are highly variable with small isoforms associated with high concentrations and pathogenic risk. Apo(a) is synthesized in the liver, although assembly of apo(a) and LDL may occur in the hepatocytes or plasma. While the uptake and clearance site of Lp(a) is poorly delineated, the kidney is the site of apo(a) fragment excretion. The structure of apo(a) has high homology to plasminogen, the zymogen for plasmin and the primary clot lysis enzyme. Apo(a) interferes with plasminogen binding to C-terminal lysines of cell surface and extracellular matrix proteins. Lp(a) and apo(a) inhibit fibrinolysis and accumulate in the vascular wall in atherosclerotic lesions. The pathogenic role of Lp(a) is not known. Small isoforms and high concentrations of Lp(a) are found in healthy octogenarians that suggest Lp(a) may also have a physiological role. Studies of Lp(a) function have been limited since it is not found in commonly studied small mammals. An important aspect of Lp(a) metabolism is the modification of circulating Lp(a), which has the potential to alter the functions of Lp(a). There are no therapeutic drugs that selectively target elevated Lp(a), but a number of possible agents are being considered. Recently, new modifiers of apo(a) synthesis have been identified. This review reports the regulation of Lp(a) metabolism and potential sites for therapeutic targets.

Indexed as

AnimalsApolipoproteins AGene Expression RegulationHumansLipoprotein(a)Receptors, LDLTissue DistributionApolipoproteins ALipoprotein(a)Receptors, LDL

Identifiers

PMID23040268
PMCPMC3547132
OpenAlexW2041093009

What OpenQuestion holds

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Registered trials

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.