Evidence map›Paper›PMID 24680834›Full record

ArticleBiochemical and biophysical research communications2014

CDKN2B expression and subcutaneous adipose tissue expandability: possible influence of the 9p21 atherosclerosis locus.

Per-Arne Svensson, Björn Wahlstrand, Maja Olsson, Philippe Froguel, Mario Falchi, Richard N Bergman, Philip G McTernan, Thomas Hedner, Lena M S Carlsson, Peter Jacobson

Open access · hybridAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Effect of 9p21.3 (lncRNA and CDKN2A/2B) variant on lipid profile.Frontiers in cardiovascular medicine · 2022
    Pooled it
  2. Article
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  5. Article
  6. Knocking DownCells · 2023
    Article
  7. Article
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  10. Article
  11. Article
  12. Long Noncoding RNAFrontiers in cardiovascular medicine · 2018
    Review
  13. Article
  14. Review
  15. Article
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

10 authors at 5 institutions in 3 countries.

Per-Arne SvenssonInstitute of Medicine, The Sahlgrenska Academy at University of Gothenburg, Sweden.
Björn WahlstrandInstitute of Medicine, The Sahlgrenska Academy at University of Gothenburg, Sweden.
Maja OlssonInstitute of Medicine, The Sahlgrenska Academy at University of Gothenburg, Sweden.
Philippe FroguelDepartment of Genomics of Common Disease, School of Public Health, Imperial College London, UK.
Mario FalchiDepartment of Genomics of Common Disease, School of Public Health, Imperial College London, UK.
Richard N BergmanDiabetes and Obesity Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Philip G McTernanDivision of Metabolic and Vascular Health, Warwick Medical School, University of Warwick, Coventry, UK.
Thomas HednerInstitute of Medicine, The Sahlgrenska Academy at University of Gothenburg, Sweden.
Lena M S CarlssonInstitute of Medicine, The Sahlgrenska Academy at University of Gothenburg, Sweden.
Peter JacobsonInstitute of Medicine, The Sahlgrenska Academy at University of Gothenburg, Sweden. Electronic address: peter.jacobson@medfak.gu.se.
University of Gothenburg · SECedars-Sinai Medical Center · USGenomics (United Kingdom) · GBImperial College London · GBUniversity of Warwick · GB

Funding

Medical Research Council G1002084Wellcome Trust
6 · The paper itself

Abstract

Risk alleles within a gene desert at the 9p21 locus constitute the most prevalent genetic determinant of cardiovascular disease. Previous research has demonstrated that 9p21 risk variants influence gene expression in vascular tissues, yet the biological mechanisms by which this would mediate atherosclerosis merits further investigation. To investigate possible influences of this locus on other tissues, we explored expression patterns of 9p21-regulated genes in a panel of multiple human tissues and found that the tumor suppressor CDKN2B was highly expressed in subcutaneous adipose tissue (SAT). CDKN2B expression was regulated by obesity status, and this effect was stronger in carriers of 9p21 risk alleles. Covariation between expression of CDKN2B and genes implemented in adipogenesis was consistent with an inhibitory effect of CDKN2B on SAT proliferation. Moreover, studies of postprandial triacylglycerol clearance indicated that CDKN2B is involved in down-regulation of SAT fatty acid trafficking. CDKN2B expression in SAT correlated with indicators of ectopic fat accumulation, including markers of hepatic steatosis. Among genes regulated by 9p21 risk variants, CDKN2B appears to play a significant role in the regulation of SAT expandability, which is a strong determinant of lipotoxicity and therefore might contribute to the development of atherosclerosis.

Indexed as

Gene Expression RegulationAdultAtherosclerosisBody Mass IndexChromosomes, Human, Pair 9Cyclin-Dependent Kinase Inhibitor p15Energy MetabolismFemaleGenetic LociHumansLipid MetabolismMaleMiddle AgedPostprandial PeriodSubcutaneous FatCyclin-Dependent Kinase Inhibitor p15Adipose tissueCDKN2BChromosome 9p21

Identifiers

PMID24680834
PMCPMC4003348
OpenAlexW2031026404

What OpenQuestion 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 OpenQuestion graph.