Evidence map›Paper›PMID 28951827›Full record

ReviewMolecular metabolism2017

Transcribing β-cell mitochondria in health and disease.

Hindrik Mulder

Open access · goldAbstract readReview
In one paragraph

Review in Molecular metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

50 citing papers in PubMed, 76 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Integrated Omics RevealPharmaceuticals (Basel, Switzerland) · 2025
    Article
  9. Identification of a novelFrontiers in oncology · 2025
    Article
  10. Review
  11. Type 2 diabetes mellitus in adults: pathogenesis, prevention and therapy.Signal transduction and targeted therapy · 2024 · on this map
    Review
  12. Article
  13. Dual role of neuroplastin in pancreatic β cells: Regulating insulin secretion and promoting islet inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

1 author at 1 institution in 1 country.

Hindrik MulderUnit of Molecular Metabolism, Lund University Diabetes Centre, Malmö, Sweden.
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe recent genome-wide association studies (GWAS) of Type 2 Diabetes (T2D) have identified the pancreatic β-cell as the culprit in the pathogenesis of the disease. Mitochondrial metabolism plays a crucial role in the processes controlling release of insulin and β-cell mass. This notion implies that mechanisms controlling mitochondrial function have the potential to play a decisive pathogenetic role in T2D. SCOPE OF THE REVIEW: This article reviews studies demonstrating that there is indeed mitochondrial dysfunction in islets in T2D, and that GWAS have identified a variant in the gene encoding transcription factor B1 mitochondrial ( MAJOR

conclusionsBased on this, it is argued that transcription and translation in mitochondria are critical processes determining mitochondrial function in β-cells in health and disease.

Indexed as

AnimalsDiabetes Mellitus, Type 2DNA-Binding ProteinsGenetic Predisposition to DiseaseGenome-Wide Association StudyGlycolysisHumansInsulinInsulin-Secreting CellsInsulin SecretionMethyltransferasesMitochondriaMitochondrial ProteinsOxidative StressTranscription FactorsDNA-Binding ProteinsInsulinMethyltransferasesMitochondrial ProteinsTFB1M protein, humanTfb1m protein, mouseTFB2M protein, humanTranscription FactorsAMPK, AMP-dependent protein kinaseATGL, adipocyte triglyceride lipaseCOX, Cytochrome c oxidaseCYTB, Cytochrome beQTL, Expression quantitative trait locusERR-α, Estrogen-related receptor-αExpression quantitative trait locus (eQTL)GDH, Glutamate dehydrogenaseGenome-wide association study (GWAS)GSIS, Glucose-stimulated insulin secretionGWAS, Genome-wide association studyHSL, Hormone-sensitive lipaseICDc, Cytosolic isocitrate dehydrogenaseInsulin secretionIsletsKATP, ATP-dependent K+-channelMitochondriaMTERF, Mitochondrial transcription termination factorND, NADH dehydrogenaseNRF, Nuclear respiratory factorNSUN4, NOP2/Sun RNA methyltransferase family member 4OXPHOS, Oxidative phosphorylationPC, Pyruvate carboxylasePDH, pyruvate dehydrogenasePGC, Peroxisome proliferator-activated receptor-γ co-activatorPOLRMT, Mitochondrial RNA polymerasePOLγ, DNA polymerase-γPPARγ, Peroxisome proliferator-activated receptor-γPRC, PGC1-related coactivatorSENP1, Sentrin/SUMO-specific protease-1SNP, Single Nucleotide PolymorphismSUR1, Sulphonylurea receptor-1T2D, Type 2 DiabetesTCA, Tricarboxylic acidTEFM, Mitochondrial transcription elongation factorTFAM, Transcription factor A mitochondrialTFB1M, Transcription factor B1 mitochondrialTFB2M, Transcription factor B2 mitochondrialβ-Cell

Identifiers

PMID28951827
PMCPMC5605719
OpenAlexW2619445100

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.