Evidence map›Paper›PMID 29782529›Full record

ArticlePloS one2018

Molecular effect of an OPTN common variant associated to Paget's disease of bone.

Iris A L Silva, Natércia Conceição, Édith Gagnon, Jacques P Brown, M Leonor Cancela, Laëtitia Michou

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 11 citations in OpenAlex.

  1. Epigenetic Regulation ofInternational journal of molecular sciences · 2025
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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

6 authors at 2 institutions in 2 countries.

Iris A L SilvaDepartment of Biomedical Sciences and Medicine, and Algarve Biomedical Center, University of Algarve, Faro, Portugal.
Natércia ConceiçãoDepartment of Biomedical Sciences and Medicine, and Algarve Biomedical Center, University of Algarve, Faro, Portugal.
Édith GagnonResearch centre of the CHU de Québec-Université Laval, Québec City, QC, Canada.
Jacques P BrownResearch centre of the CHU de Québec-Université Laval, Québec City, QC, Canada.
M Leonor CancelaDepartment of Biomedical Sciences and Medicine, and Algarve Biomedical Center, University of Algarve, Faro, Portugal.
Laëtitia MichouResearch centre of the CHU de Québec-Université Laval, Québec City, QC, Canada.ORCID 0000-0002-8364-4164
Algarve Biomedical Center · PTUniversité Laval · CA

Funding

Canadian Institutes for Health Research MOP130457
6 · The paper itself

Abstract

Paget's disease of bone (PDB) is a chronic bone disorder and although genetic factors appear to play an important role in its pathogenesis, to date PDB causing mutations were identified only in the Sequestosome 1 (SQSTM1) gene at the PDB3 locus. PDB6 locus, also previously linked to PDB, contains several candidate genes for metabolic bone diseases. We focused our analysis in the most significantly associated variant with PDB, within the Optineurin (OPTN) gene, i.e. the common variant rs1561570. Although it was previously shown to be strongly associated with PDB in several populations, its contribution to PDB pathogenesis remains unclear. In this study we have shown that rs1561570 may contribute to PDB since its T allele results in the loss of a methylation site in patients' DNA, leading to higher levels of OPTN gene expression and a corresponding increase in protein levels in patients' osteoclasts. This increase in OPTN expression leads to higher levels of NF-κB translocation into the nucleus and increasing expression of its target genes, which may contribute to the overactivity of osteoclasts observed in PDB. We also reported a tendency for a more severe clinical phenotype in the presence of a haplotype containing the rs1561570 T allele, which appear to be re-enforced with the presence of the SQSTM1/P392L mutation. In conclusion, our work provides novel insight towards understanding the functional effects of this variant, located in OPTN intron 7, and its implication in the contribution to PDB pathogenesis.

Indexed as

Active Transport, Cell NucleusAllelesAutophagyBone ResorptionCell Cycle ProteinsCell DifferentiationCell LineDNA MethylationGenetic Association StudiesGenetic Predisposition to DiseaseGenetic VariationHaplotypesHumansIntronsMembrane Transport ProteinsMutationCell Cycle ProteinsMembrane Transport ProteinsNF-kappa BOPTN protein, humanSequestosome-1 ProteinSQSTM1 protein, humanTranscription Factor TFIIIA

Identifiers

PMID29782529
PMCPMC5962077
OpenAlexW2803192810

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.