Evidence map›Paper›PMID 26873508›Full record

ReviewDiabetologia2016

Mitochondrial network regulation and its potential interference with inflammatory signals in pancreatic beta cells.

Simone Baltrusch

Abstract readReview
PubMed Publisher
In one paragraph

Review in Diabetologia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Asiatic acid improves insulin secretion ofZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023
    Article
  6. Role of mitochondrial DNA in diabetes Mellitus Type I and Type II.Saudi journal of biological sciences · 2022
    Review
  7. Article
  8. Review
  9. The Role of Mitochondrial Mutations and Chronic Inflammation in Diabetes.International journal of molecular sciences · 2021
    Review
  10. The Role of Oxidative Stress in Pancreatic β Cell Dysfunction in Diabetes.International journal of molecular sciences · 2021
    Review
  11. Article
  12. Article
  13. Molecular Machinery and Pathophysiology of Mitochondrial Dynamics.Frontiers in cell and developmental biology · 2021
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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.

Simone BaltruschInstitute of Medical Biochemistry and Molecular Biology, University of Rostock, Schillingallee 70, 18057, Rostock, Germany. simone.baltrusch@med.uni-rostock.de.
University of Rostock · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria fulfil multiple tasks in nutrient metabolism, energy production, redox homeostasis and stress response, and are essential for pancreatic beta cell function. The dynamism and health of the mitochondrial network is regulated by fission- and fusion-triggering factors and by a quality control system that removes dysfunctional organelles. Alongside the role of mitochondria in regulating apoptotic cell death mediated primarily via production of reactive oxygen species and release of cytochrome c, there is evidence of other links between mitochondria and inflammation that have implications for cell viability. This review briefly outlines two pathways that are potentially vital for pancreatic beta cell function. The first concerns the regulation of Parkin, a protein that acts, not only as a central player in regulating mitophagy, but also as an activator of the NF-ĸB pathway. The fact that expression of optic atrophy protein 1 (OPA1), a mitochondrial fusion inducer and master mitochondrial cristae biogenetic factor, is increased following NF-ĸB activation highlights a point of mitochondrial control that might be influenced by TNFα signalling. A second axis of interest is suggested by IL-6-mediated upregulation of the fission inducer FIS1 alongside downregulation of mitofusin 2 (MFN2), a guard of mitochondrial fusion and metabolism and an inhibitor of apoptosis. This review summarises a presentation given at the 'Islet inflammation in type 2 diabetes' symposium at the 2015 annual meeting of the EASD. It is accompanied two other reviews on topics from this symposium (by Marc Donath, DOI: 10.1007/s00125-016-3873-z , and Jerry Nadler and colleagues, DOI: 10.1007/s00125-016-3890-y ) and a commentary by the Session Chair, Piero Marchetti (DOI: 10.1007/s00125-016-3875-x ).

Indexed as

AnimalsHumansInflammationInsulin-Secreting CellsMitochondriaSignal TransductionFission protein 1InflammationMitochondrial dynamicsMitochondrial networkMitofusinsNF-ĸB pathwayOptic atrophy protein 1Pancreatic beta cellsParkinReview

Identifiers

PMID26873508
OpenAlexW2254554875

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.