Evidence map›Paper›PMID 21749171›Full record

ReviewMetabolic syndrome and related disorders2011

Lipoprotein(a): genotype-phenotype relationship and impact on atherogenic risk.

Byambaa Enkhmaa, Erdembileg Anuurad, Wei Zhang, Tina Tran, Lars Berglund

Abstract readReview
In one paragraph

Review in Metabolic syndrome and related disorders, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.7field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 49 citations in OpenAlex.

  1. Trial
  2. Journal of the American Heart Association · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Lipoprotein(a) as a Risk Factor for Cardiovascular Diseases: Pathophysiology and Treatment Perspectives.International journal of environmental research and public health · 2023
    Review
  9. Article
  10. Review
  11. Untying the correlation between apolipoproteins and rheumatoid arthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Review
  12. Article
  13. Lack of Correlation of Carotid Intima-Media Index and Peripheral Artery Disease.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2018
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review
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

5 authors at 2 institutions in 1 country.

Byambaa EnkhmaaDepartment of Medicine, University of California, Davis, USA.
Erdembileg Anuurad
Wei Zhang
Tina Tran
Lars Berglund
University of California, Davis · USVA Northern California Health Care System · US

Funding

UC DAVIS CLINICAL AND TRANSLATIONAL SCIENCE CENTER: BPCAUL1RR024146 · NCRR · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERGLUND, LARS F · 2006 to 2011
$27.0M
Regulation of Lipoprotein(a) Metabolism in Humans with Reference to EthnicityR01HL062705 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI BERGLUND, LARS F · 2000 to 2011
$2.9M
NCRR NIH HHS RR 024146NHLBI NIH HHS HL 62705
6 · The paper itself

Abstract

In 2010, more than 45 years after the initial discovery of lipoprotein(a) [Lp(a)] by Kare Berg, an European Atherosclerosis Society Consensus Panel recommended screening for elevated Lp(a) in people at moderate to high risk of atherosclerotic cardiovascular disease (CVD). This recommendation was based on extensive epidemiological findings demonstrating a significant association between elevated plasma Lp(a) levels and coronary heart disease, myocardial infarction, and stroke. In addition to those patients considered to be at moderate to high risk of heart disease, statin-treated patients with recurrent heart disease were also identified as targeted for screening of elevated Lp(a) levels. Taken together, recent findings have significantly strengthened the notion of Lp(a) as a causal risk factor for CVD. It is well established that Lp(a) levels are largely determined by the size of the apolipoprotein a [apo(a)] gene; however, recent studies have identified several other LPA gene polymorphisms that have significant associations with an elevated Lp(a) level and a reduced copy number of K4 repeats. In addition, the contribution of other genes in regulating Lp(a) levels has been described. Besides the strong genetic regulation, new evidence has emerged regarding the impact of inflammation as a modulator of Lp(a) risk factor properties. Thus, oxidized phospholipids that possess a strong proinflammatory potential are preferentially carried on Lp(a) particles. Collectively, these findings point to the importance of both phenotypic and genotypic factors in influencing apo(a) proatherogenic properties. Therefore, studies taking both of these factors into account determining the amount of Lp(a) associated with each individual apo(a) size allele are valuable tools when assessing a risk factor role of Lp(a).

Indexed as

AllelesAtherosclerosisCoronary DiseaseGenetic Association StudiesGenetic Predisposition to DiseaseHumansLipoprotein(a)Models, BiologicalPolymorphism, GeneticRisk FactorsLipoprotein(a)

Identifiers

PMID21749171
PMCPMC3225061
OpenAlexW1979502189

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.