Evidence map›Paper›PMID 25010439›Full record

ReviewCurrent opinion in rheumatology2014

Advances in lupus genetics and epigenetics.

Yun Deng, Betty P Tsao

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in rheumatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
14.5field-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

55 citing papers in PubMed, 119 citations in OpenAlex.

  1. Review
  2. Article
  3. RareInnovation (Cambridge (Mass.)) · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Precision medicine in systemic lupus erythematosus.Nature reviews. Rheumatology · 2023
    Review
  9. Review
  10. Article
  11. Review
  12. Lupus, DNA Methylation, and Air Pollution: A Malicious Triad.International journal of environmental research and public health · 2022
    Review
  13. Genotype Triad forDiagnostics (Basel, Switzerland) · 2022
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Neutrophils in the Pathogenesis of Rheumatic Diseases: Fueling the Fire.Clinical reviews in allergy & immunology · 2021
    Review
  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

2 authors at 1 institution in 1 country.

Yun DengDivision of Rheumatology, David Geffen School of Medicine, University of California, Los Angeles, California, USA.
Betty P Tsao
University of California, Los Angeles · US

Funding

CHROMOSOME REGIONS LINKED TO SLE IN MULTIPLEX FAMILIESR01AR043814 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TSAO, BETTY P · 1997 to 2012
$5.7M
Association of Androgen Receptor Polymorphisms with Damage in SLER21AR065626 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TSAO, BETTY P · 2013 to 2014
$357k
NIAMS NIH HHS R01 AR043814NIAMS NIH HHS R01AR043814NIAMS NIH HHS R21 AR065626NIAMS NIH HHS R21AR065626
6 · The paper itself

Abstract

purpose of reviewGenome-wide association studies have identified more than 50 robust loci associated with systemic lupus erythematosus (SLE) susceptibility, and follow-up studies help reveal candidate causative genetic variants and their biological relevance contributing to the development of SLE. Epigenetic modulation is emerging as an important mechanism for understanding how the implicated genes interact with environmental factors. We review recent progress toward identifying causative variants of SLE-associated loci and epigenetic impact on lupus, especially genetic-epigenetic interactions that modulate expression levels of SLE susceptibility genes. RECENT

findingsA few SLE-risk loci have been refined to localize likely causative variants responsible for the observed genome-wide association study signals. Few of such variants disrupt coding sequences resulting in gain or loss of function for the encoded protein, whereas most fall in noncoding regions with potential to regulate gene expression through alterations in transcriptional activity, splicing, mRNA stability and epigenetic modifications. Multiple key pathways related to the SLE pathogenesis have been indicated by the identified genetic risk factors, including type I interferon signaling pathway that can also be regulated by epigenetic changes occurred in SLE. SUMMARY: These findings provide novel insights into the disease pathogenesis and promise better diagnostic accuracy and new therapeutic targets for patient management.

Indexed as

Epigenesis, GeneticAnimalsAntigen-Antibody ComplexB-LymphocytesDNA MethylationGene-Environment InteractionGenetic Predisposition to DiseaseGenetic VariationGenome-Wide Association StudyHistonesHumansInterferon Type ILupus Erythematosus, SystemicMicroRNAsNADPH OxidasesNF-kappa BAntigen-Antibody ComplexHistonesInterferon Type IMicroRNAsNADPH OxidasesNF-kappa BReactive Oxygen Species

Identifiers

PMID25010439
PMCPMC4222581
OpenAlexW2019536120

What OpenQuestion holds

Textmetadata
LicenceTDM
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.