Evidence map›Paper›PMID 28464818›Full record

ArticleRespiratory research2017

Sulfatase modifying factor 1 (SUMF1) is associated with Chronic Obstructive Pulmonary Disease.

Julie Weidner, Linnea Jarenbäck, Kim de Jong, Judith M Vonk, Maarten van den Berge, Corry-Anke Brandsma, H Marike Boezen, Don Sin, Yohan Bossé, David Nickle and 5 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Respiratory research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. International journal of molecular sciences · 2025
    Trial
  2. The Genetics behind Sulfation: Impact on Airway Remodeling.Journal of personalized medicine · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. 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

15 authors at 7 institutions in 4 countries.

Julie WeidnerRespiratory Medicine and Allergology, Department of Clinical Sciences Lund, BMC, D12, Lund University, Skåne University Hospital, 221 84, Lund, Sweden.
Linnea JarenbäckRespiratory Medicine and Allergology, Department of Clinical Sciences Lund, BMC, D12, Lund University, Skåne University Hospital, 221 84, Lund, Sweden.
Kim de JongUniversity Medical Center Groningen, GRIAC (Groningen Research Institute for Asthma and COPD), Department of Epidemiology, University of Groningen, Groningen, The Netherlands.
Judith M VonkUniversity Medical Center Groningen, GRIAC (Groningen Research Institute for Asthma and COPD), Department of Epidemiology, University of Groningen, Groningen, The Netherlands.
Maarten van den BergeUniversity Medical Center Groningen, Department of Pulmonology, GRIAC (Groningen Research Institute for Asthma and COPD), University of Groningen, Groningen, The Netherlands.
Corry-Anke BrandsmaUniversity Medical Center Groningen, Department of Pulmonology, GRIAC (Groningen Research Institute for Asthma and COPD), University of Groningen, Groningen, The Netherlands.
H Marike BoezenUniversity Medical Center Groningen, GRIAC (Groningen Research Institute for Asthma and COPD), Department of Epidemiology, University of Groningen, Groningen, The Netherlands.
Don SinDepartment of Medicine (Respirology), University of British Columbia, Centre for Heart Lung Innovation, Vancouver, Canada.
Yohan BosséDepartment of Molecular Medicine, Institut universitaire de cardiologie et de pneumologie de Québec, Laval University, Québec, Canada.
David NickleGenetics and Pharmacogenomics (GpGx), Merck Research Laboratories, Boston, MA, USA.
Jaro AnkerstRespiratory Medicine and Allergology, Department of Clinical Sciences Lund, BMC, D12, Lund University, Skåne University Hospital, 221 84, Lund, Sweden.
Leif BjermerRespiratory Medicine and Allergology, Department of Clinical Sciences Lund, BMC, D12, Lund University, Skåne University Hospital, 221 84, Lund, Sweden.
Dirkje S PostmaUniversity Medical Center Groningen, Department of Pulmonology, GRIAC (Groningen Research Institute for Asthma and COPD), University of Groningen, Groningen, The Netherlands.
Alen FaizUniversity Medical Center Groningen, Department of Pulmonology, GRIAC (Groningen Research Institute for Asthma and COPD), University of Groningen, Groningen, The Netherlands.
Ellen TufvessonRespiratory Medicine and Allergology, Department of Clinical Sciences Lund, BMC, D12, Lund University, Skåne University Hospital, 221 84, Lund, Sweden. Ellen.Tufvesson@med.lu.se.
University Medical Center Groningen · NLLund University · SEUniversity of Groningen · NLSkåne University Hospital · SEInstitut universitaire de cardiologie et de pneumologie de Québec · CAMerck & Co., Inc., Rahway, NJ, USA (United States) · USUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIt has been observed that mice lacking the sulfatase modifying factor (Sumf1) developed an emphysema-like phenotype. However, it is unknown if SUMF1 may play a role in Chronic Obstructive Pulmonary Disease (COPD) in humans. The aim was to investigate if the expression and genetic regulation of SUMF1 differs between smokers with and without COPD.

methodsSUMF1 mRNA was investigated in sputum cells and whole blood from controls and COPD patients (all current or former smokers). Expression quantitative trait loci (eQTL) analysis was used to investigate if single nucleotide polymorphisms (SNPs) in SUMF1 were significantly associated with SUMF1 expression. The association of SUMF1 SNPs with COPD was examined in a population based cohort, Lifelines. SUMF1 mRNA from sputum cells, lung tissue, and lung fibroblasts, as well as lung function parameters, were investigated in relation to genotype.

resultsCertain splice variants of SUMF1 showed a relatively high expression in lung tissue compared to many other tissues. SUMF1 Splice variant 2 and 3 showed lower levels in sputum cells from COPD patients as compared to controls. Twelve SNPs were found significant by eQTL analysis and overlapped with the array used for genotyping of Lifelines. We found alterations in mRNA expression in sputum cells and lung fibroblasts associated with SNP rs11915920 (top hit in eQTL), which validated the results of the lung tissue eQTL analysis. Of the twelve SNPs, two SNPs, rs793391 and rs308739, were found to be associated with COPD in Lifelines. The SNP rs793391 was also confirmed to be associated with lung function changes.

conclusionsWe show that SUMF1 expression is affected in COPD patients compared to controls, and that SNPs in SUMF1 are associated with an increased risk of COPD. Certain COPD-associated SNPs have effects on either SUMF1 gene expression or on lung function. Collectively, this study shows that SUMF1 is associated with an increased risk of developing COPD.

Indexed as

AgedBiomarkersFemaleGenetic Association StudiesGenetic MarkersGenetic Predisposition to DiseaseHumansMaleOxidoreductases Acting on Sulfur Group DonorsPolymorphism, Single NucleotidePrevalencePulmonary Disease, Chronic ObstructiveReproducibility of ResultsRisk FactorsSensitivity and SpecificitySmokingBiomarkersGenetic MarkersOxidoreductases Acting on Sulfur Group DonorsSulfatasesSUMF1 protein, humanChronic obstructive pulmonary diseaseLung fibroblastSingle nucleotide polymorphismSputumSulfatase modifying factor 1

Identifiers

PMID28464818
PMCPMC5414362
OpenAlexW2611651602

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.