Evidence map›Paper›PMID 26075204›Full record

ReviewFrontiers in cell and developmental biology2015

Redox interplay between mitochondria and peroxisomes.

Celien Lismont, Marcus Nordgren, Paul P Van Veldhoven, Marc Fransen

Abstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
–field-weighted citation impact
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

117 citing papers in PubMed.

  1. Article
  2. Macrophage peroxisomes at the crossroads of inflammation.Immunometabolism (Cobham, Surrey) · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

57 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

4 authors.

Celien LismontLaboratory of Lipid Biochemistry and Protein Interactions, Department of Cellular and Molecular Medicine, KU Leuven - University of Leuven Leuven, Belgium.
Marcus NordgrenLaboratory of Lipid Biochemistry and Protein Interactions, Department of Cellular and Molecular Medicine, KU Leuven - University of Leuven Leuven, Belgium.
Paul P Van VeldhovenLaboratory of Lipid Biochemistry and Protein Interactions, Department of Cellular and Molecular Medicine, KU Leuven - University of Leuven Leuven, Belgium.
Marc FransenLaboratory of Lipid Biochemistry and Protein Interactions, Department of Cellular and Molecular Medicine, KU Leuven - University of Leuven Leuven, Belgium.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reduction-oxidation or "redox" reactions are an integral part of a broad range of cellular processes such as gene expression, energy metabolism, protein import and folding, and autophagy. As many of these processes are intimately linked with cell fate decisions, transient or chronic changes in cellular redox equilibrium are likely to contribute to the initiation and progression of a plethora of human diseases. Since a long time, it is known that mitochondria are major players in redox regulation and signaling. More recently, it has become clear that also peroxisomes have the capacity to impact redox-linked physiological processes. To serve this function, peroxisomes cooperate with other organelles, including mitochondria. This review provides a comprehensive picture of what is currently known about the redox interplay between mitochondria and peroxisomes in mammals. We first outline the pro- and antioxidant systems of both organelles and how they may function as redox signaling nodes. Next, we critically review and discuss emerging evidence that peroxisomes and mitochondria share an intricate redox-sensitive relationship and cooperate in cell fate decisions. Key issues include possible physiological roles, messengers, and mechanisms. We also provide examples of how data mining of publicly-available datasets from "omics" technologies can be a powerful means to gain additional insights into potential redox signaling pathways between peroxisomes and mitochondria. Finally, we highlight the need for more studies that seek to clarify the mechanisms of how mitochondria may act as dynamic receivers, integrators, and transmitters of peroxisome-derived mediators of oxidative stress. The outcome of such studies may open up exciting new avenues for the community of researchers working on cellular responses to organelle-derived oxidative stress, a research field in which the role of peroxisomes is currently highly underestimated and an issue of discussion.

Indexed as

antioxidant systemsinterorganellar cross-talkmitochondriaoxidative stressperoxisomespro-oxidant systemsredox signaling

Identifiers

PMID26075204
PMCPMC4444963

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.