Evidence map›Paper›PMID 23029600›Full record

ReviewOxidative medicine and cellular longevity2012

Mitochondrial hormesis in pancreatic β cells: does uncoupling protein 2 play a role?

Ning Li, Suzana Stojanovski, Pierre Maechler

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Review
  3. Role of Mitophagy in Regulating Intestinal Oxidative Damage.Antioxidants (Basel, Switzerland) · 2023
    Review
  4. The Pancreatic β-Cell: The Perfect Redox System.Antioxidants (Basel, Switzerland) · 2021
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. When less is more: hormesis against stress and disease.Microbial cell (Graz, Austria) · 2014
    Review
  13. Hormesis in aging and neurodegeneration-a prodigy awaiting dissection.International journal of molecular sciences · 2013
    Review
  14. Oxidative stress and the ageing endocrine system.Nature reviews. Endocrinology · 2013
    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

3 authors at 1 institution in 1 country.

Ning LiDepartment of Cell Physiology and Metabolism, University of Geneva Medical Centre, Rue Michel-Servet 1, 1211 Geneva 4, Switzerland. ning.li@unige.ch
Suzana Stojanovski
Pierre Maechler
University of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In pancreatic β cells, mitochondrial metabolism translates glucose sensing into signals regulating insulin secretion. Chronic exposure of β cells to excessive nutrients, namely, glucolipotoxicity, impairs β-cell function. This is associated with elevated ROS production from overstimulated mitochondria. Mitochondria are not only the major source of cellular ROS, they are also the primary target of ROS attacks. The mitochondrial uncoupling protein UCP2, even though its uncoupling properties are debated, has been associated with protective functions against ROS toxicity. Hormesis, an adaptive response to cellular stresses, might contribute to the protection against β-cell death, possibly limiting the development of type 2 diabetes. Mitochondrial hormesis, or mitohormesis, is a defense mechanism observed in ROS-induced stress-responses by mitochondria. In β cells, mitochondrial damages induced by sublethal exogenous H(2)O(2) can induce secondary repair and defense mechanisms. In this context, UCP2 is a marker of mitohormesis, being upregulated following stress conditions. When overexpressed in nonstressed naïve cells, UCP2 confers resistance to oxidative stress. Whether treatment with mitohormetic inducers is sufficient to restore or ameliorate secretory function of β cells remains to be determined.

Indexed as

AnimalsDiabetes Mellitus, Type 2GlucoseHormesisHumansInsulinInsulin-Secreting CellsInsulin SecretionIon ChannelsMitochondriaMitochondrial ProteinsOxidative StressReactive Oxygen SpeciesUncoupling Protein 2GlucoseInsulinIon ChannelsMitochondrial ProteinsReactive Oxygen SpeciesUCP2 protein, humanUncoupling Protein 2

Identifiers

PMID23029600
PMCPMC3458419
OpenAlexW1998084948

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.