Evidence map›Paper›PMID 29080939›Full record

ArticleHuman cell2018

A common variant of MAF/c-MAF, transcriptional factor gene in the kidney, is associated with gout susceptibility.

Toshihide Higashino, Hirotaka Matsuo, Yukinori Okada, Hiroshi Nakashima, Seiko Shimizu, Masayuki Sakiyama, Shin Tadokoro, Akiyoshi Nakayama, Makoto Kawaguchi, Mako Komatsu and 5 more

Open access · hybridAbstract read
PubMed Publisher
In one paragraph

Article in Human cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 38% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. 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 4 institutions in 1 country.

Toshihide HigashinoDepartment of Integrative Physiology and Bio-Nano Medicine, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, 359-8513, Japan.
Hirotaka MatsuoDepartment of Integrative Physiology and Bio-Nano Medicine, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, 359-8513, Japan. hmatsuo@ndmc.ac.jp.
Yukinori OkadaDepartment of Statistical Genetics, Osaka University Graduate School of Medicine, Osaka, Japan.
Hiroshi NakashimaDepartment of Preventive Medicine and Public Health, National Defense Medical College, Tokorozawa, Japan.
Seiko ShimizuDepartment of Integrative Physiology and Bio-Nano Medicine, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, 359-8513, Japan.
Masayuki SakiyamaDepartment of Integrative Physiology and Bio-Nano Medicine, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, 359-8513, Japan.
Shin TadokoroDepartment of Integrative Physiology and Bio-Nano Medicine, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, 359-8513, Japan.
Akiyoshi NakayamaDepartment of Integrative Physiology and Bio-Nano Medicine, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, 359-8513, Japan.
Makoto KawaguchiDepartment of Integrative Physiology and Bio-Nano Medicine, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, 359-8513, Japan.
Mako KomatsuDepartment of Integrative Physiology and Bio-Nano Medicine, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, 359-8513, Japan.
Asahi HishidaDepartment of Preventive Medicine, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
Masahiro NakatochiStatistical Analysis Section, Center for Advanced Medicine and Clinical Research, Nagoya University Hospital, Nagoya, Aichi, Japan.
Hiroshi OoyamaRyougoku East Gate Clinic, Tokyo, Japan.
Junko ImakiDepartment of Developmental Anatomy and Regenerative Biology, National Defense Medical College, Tokorozawa, Saitama, Japan.
Nariyoshi ShinomiyaDepartment of Integrative Physiology and Bio-Nano Medicine, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, 359-8513, Japan.
National Defense Medical College · JPNagoya University · JPNagoya University Hospital · JPOsaka University · JP

Funding

Ministry of Education, Culture, Sports, Science and Technology 15K15227Ministry of Education, Culture, Sports, Science and Technology 16H06277Ministry of Education, Culture, Sports, Science and Technology 16H06279Ministry of Education, Culture, Sports, Science and Technology 17015018Ministry of Education, Culture, Sports, Science and Technology 221S0001Ministry of Education, Culture, Sports, Science and Technology 221S0002Ministry of Education, Culture, Sports, Science and Technology 25293145
6 · The paper itself

Abstract

Gout is a multifactorial disease characterized by acute inflammatory arthritis, and it is caused as a consequence of hyperuricemia. A recent meta-analysis of genome-wide association studies has newly identified the relationship between serum uric acid (SUA) levels and rs889472, a single nucleotide polymorphism of musculoaponeurotic fibrosarcoma oncogene (MAF/c-MAF). However, it remained unclear whether rs889472 is associated with gout susceptibility. In the present study, we investigate the association between c-MAF rs889472 and gout in Japanese male population. We genotyped 625 male patients who were clinically diagnosed as gout and 1221 male control subjects without hyperuricemia or a history of gout by TaqMan method. As a result, the major allele (C), which reportedly increases SUA levels, had a higher frequency in the gout cases (58.8%) than in the controls (55.0%). A logistic regression analysis showed a significant association between rs889472 and gout (p = 0.029, odds ratio = 1.17; 95% confidence interval 1.02-1.34). C-MAF is reported as a pivotal transcriptional factor in the development and differentiation of renal proximal tubular cells. Because urate is mainly regulated in renal proximal tubular cells, c-MAF may have an important role in urate regulation in the kidney and influence not only SUA but also gout susceptibility. Our finding shows that rs889472 of c-MAF is associated with gout susceptibility.

Indexed as

Genetic Association StudiesAdultAsian PeopleCell DifferentiationGene FrequencyGenetic Predisposition to DiseaseGoutHumansKidney Tubules, ProximalLogistic ModelsMaleMiddle AgedProto-Oncogene Proteins c-mafTranscription FactorsUric AcidMAF protein, humanProto-Oncogene Proteins c-mafTranscription FactorsUric Acidc-MAFGouty arthritisHyperuricemiaMAFSingle-nucleotide polymorphism (SNP)

Identifiers

PMID29080939
OpenAlexW2766177569

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.