Evidence map›Paper›PMID 23785334›Full record

ArticleFrontiers in physiology2013

Peroxisome degradation in mammals: mechanisms of action, recent advances, and perspectives.

Marcus Nordgren, Bo Wang, Oksana Apanasets, Marc Fransen

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.5field-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

33 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. The Peroxisome-Autophagy Redox Connection: A Double-Edged Sword?Frontiers in cell and developmental biology · 2021
    Review
  8. Article
  9. The cell biology of the retinal pigment epithelium.Progress in retinal and eye research · 2020
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. The Peroxisome-Mitochondria Connection: How and Why?International journal of molecular sciences · 2017
    Review
  17. Review
  18. Aspirin increases mitochondrial fatty acid oxidation.Biochemical and biophysical research communications · 2017
    Article
  19. Comparison of Transcriptome Between Type 2 Diabetes Mellitus and Impaired Fasting Glucose.Medical science monitor : international medical journal of experimental and clinical research · 2016
    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

4 authors at 1 institution in 1 country.

Marcus NordgrenLaboratory of Lipid Biochemistry and Protein Interactions, Department of Cellular and Molecular Medicine, Katholieke Universiteit Leuven Leuven, Vlaams-Brabant, Belgium.
Bo Wang
Oksana Apanasets
Marc Fransen
KU Leuven · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Peroxisomes are remarkably dynamic organelles that participate in a diverse array of cellular processes, including the metabolism of lipids and reactive oxygen species. In order to regulate peroxisome function in response to changing nutritional and environmental stimuli, new organelles need to be formed and superfluous and dysfunctional organelles have to be selectively removed. Disturbances in any of these processes have been associated with the etiology and progression of various congenital neurodegenerative and age-related human disorders. The aim of this review is to critically explore our current knowledge of how peroxisomes are degraded in mammalian cells and how defects in this process may contribute to human disease. Some of the key issues highlighted include the current concepts of peroxisome removal, the peroxisome quality control mechanisms, the initial triggers for peroxisome degradation, the factors for dysfunctional peroxisome recognition, and the regulation of peroxisome homeostasis. We also dissect the functional and mechanistic relationship between different forms of selective organelle degradation and consider how lysosomal dysfunction may lead to defects in peroxisome turnover. In addition, we draw lessons from studies on other organisms and extrapolate this knowledge to mammals. Finally, we discuss the potential pathological implications of dysfunctional peroxisome degradation for human health.

Indexed as

autophagylysosomesorganelle quality controlorganelle turnoverperoxisomespexophagyprotein importreactive oxygen species

Identifiers

PMID23785334
PMCPMC3682127
OpenAlexW1993630264

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.