Evidence map›Paper›PMID 16767843›Full record

ReviewCurrent atherosclerosis reports2006

Human genetics of variation in high-density lipoprotein cholesterol.

Atif Qasim, Daniel J Rader

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current atherosclerosis reports, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. A PolynesianHGG advances · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  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

2 authors at 1 institution in 1 country.

Atif QasimInstitute for Translational Medicine and Therapeutics, University of Pennsylvania School of Medicine, 421 Curie Boulevard, Philadelphia, PA 19104, USA.
Daniel J Rader
Translational Therapeutics (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Longitudinal population studies have confirmed plasma levels of high-density lipoprotein (HDL) cholesterol to be an important inverse coronary risk factor. Although environmental influences are known to regulate HDL cholesterol levels, genetic factors are also known to be important, and over 25 candidate genes have been proposed to be associated with variation in HDL cholesterol levels. A variety of monogenic conditions of extremely low or high HDL cholesterol has helped to delineate the physiology of HDL cholesterol metabolism in humans, which has led to the development of new therapeutic approaches to HDL cholesterol. However, most causes of genetic variation in HDL cholesterol in the general population are likely oligogenic or polygenic. We review the monogenic disorders associated with both high and low HDL cholesterol and the relevance of mutations and polymorphisms in these genes to variation in HDL cholesterol levels in the general population.

Indexed as

Genetic Predisposition to DiseaseGenetic VariationApolipoprotein A-ICholesterol, HDLHumansLipaseLiverModels, BiologicalMutationPolymorphism, GeneticRisk FactorsApolipoprotein A-ICholesterol, HDLLipase

Identifiers

PMID16767843
OpenAlexW1990735113

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.