Evidence map›Paper›PMID 25500951›Full record

ArticleDiabetologia2015

MafA is critical for maintenance of the mature beta cell phenotype in mice.

Wataru Nishimura, Satoru Takahashi, Kazuki Yasuda

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

72 citing papers in PubMed, 129 citations in OpenAlex.

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  13. An Insight into Vital Genes Responsible for β-cell Formation.Advances in experimental medicine and biology · 2024
    Article
  14. Editorial: Pancreatic beta-cell dedifferentiation.Frontiers in endocrinology · 2024
    Article
  15. Advanced therapy to cure diabetes: mission impossible is now possible?Frontiers in cell and developmental biology · 2024
    Review
  16. Review
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12 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Wataru NishimuraDepartment of Metabolic Disorders, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, 1-21-1 Toyama, Shinjuku-ku, Tokyo, 162-8655, Japan, wnishimura@jichi.ac.jp.
Satoru Takahashi
Kazuki Yasuda
National Center for Global Health and Medicine · JPUniversity of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisThe plasticity of adult somatic cells allows for their dedifferentiation or conversion to different cell types, although the relevance of this to disease remains elusive. Perturbation of beta cell identity leading to dedifferentiation may be implicated in the compromised functions of beta cells in diabetes, which is a current topic of islet research. This study aims to investigate whether or not v-Maf musculoaponeurotic fibrosarcoma oncogene family, protein A (MafA), a mature beta cell marker, is involved in maintaining mature beta cell phenotypes.

methodsThe fate and gene expression of beta cells were analysed in Mafa knockout (KO) mice and mouse models of diabetes in which the expression of MafA was reduced in the majority of beta cells.

resultsLoss of MafA reduced the beta to alpha cell ratio in pancreatic islets without elevating blood glucose to diabetic levels. Lineage tracing analyses showed reduced/lost expression of insulin in most beta cells, with a minority of the former beta cells converted to glucagon-expressing cells in Mafa KO mice. The upregulation of genes that are normally repressed in mature beta cells or transcription factors that are transiently expressed in endocrine progenitors was identified in Mafa KO islets as a hallmark of dedifferentiation. The compromised beta cells in db/db and multiple low-dose streptozotocin mice underwent similar dedifferentiation with expression of Mafb, which is expressed in immature beta cells. CONCLUSIONS/

interpretationThe maturation factor MafA is critical for the homeostasis of mature beta cells and regulates cell plasticity. The loss of MafA in beta cells leads to a deeper loss of cell identity, which is implicated in diabetes pathology.

Indexed as

AnimalsGlucagon-Secreting CellsImmunohistochemistryIslets of LangerhansMafB Transcription FactorMaf Transcription FactorsMaf Transcription Factors, LargeMiceMice, KnockoutMicroscopy, Electron, TransmissionReverse Transcriptase Polymerase Chain ReactionMafa protein, mouseMafB Transcription FactorMaf Transcription FactorsMaf Transcription Factors, Large

Identifiers

PMID25500951
OpenAlexW1977766265

What OpenQuestion holds

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Registered trials

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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.