Evidence map›Paper›PMID 25239010›Full record

ArticleMolecular and cellular neurosciences2014

Mitochondria-derived reactive oxygen species mediate caspase-dependent and -independent neuronal deaths.

Meagan J McManus, Michael P Murphy, James L Franklin

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular neurosciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Oxphos targeting ofFrontiers in oncology · 2025
    Article
  3. Review
  4. PET Imaging with [Antioxidants (Basel, Switzerland) · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. New insights into targeting mitochondria in ischemic injury.Apoptosis : an international journal on programmed cell death · 2021
    Review
  9. Review
  10. Article
  11. Lactate Dehydrogenase Inhibition With Oxamate Exerts Bone Anabolic Effect.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Neuronal Dysfunction Associated with Cholesterol Deregulation.International journal of molecular sciences · 2018
    Article
  18. Article
  19. The Ying and Yang of Adenosine AMolecular neurobiology · 2018
    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

3 authors at 3 institutions in 2 countries.

Meagan J McManusCenter of Mitochondrial and Epigenomic Medicine, Children's Hospital of Philadelphia, Colket Translational Research Building, 3501 Civic Center Blvd, Room 6100, Philadelphia, PA 19104, USA. Electronic address: megangm@gmail.com.
Michael P MurphyMRC Mitochondrial Biology Unit, Wellcome Trust/MRC Building, Hills Road, Cambridge CB2 0XY, UK. Electronic address: michael.murphy@mrc-mbu.cam.ac.uk.
James L FranklinDepartment of Pharmaceutical and Biomedical Sciences, The University of Georgia College of Pharmacy, 357 Wilson Pharmacy, Athens, GA 30602, USA. Electronic address: jfrankli@rx.uga.edu.
Children's Hospital of Philadelphia · USMRC Mitochondrial Biology Unit · GBUniversity of Georgia · US

Funding

Free Radicals and Mitochondria in Neuronal ApoptosisR01NS037110 · NINDS · UNIVERSITY OF WISCONSIN MADISON · PI FRANKLIN, JAMES LEE · 2004 to 2007
$1.1M
Medical Research Council MC_U105663142NINDS NIH HHS R01 NS037110NINDS NIH HHS R01NS37110
6 · The paper itself

Abstract

Mitochondrial dysfunction and oxidative stress are implicated in many neurodegenerative diseases. Mitochondria-targeted drugs that effectively decrease oxidative stress, protect mitochondrial energetics, and prevent neuronal loss may therefore lend therapeutic benefit to these currently incurable diseases. To investigate the efficacy of such drugs, we examined the effects of mitochondria-targeted antioxidants MitoQ10 and MitoE2 on neuronal death induced by neurotrophin deficiency. Our results indicate that MitoQ10 blocked apoptosis by preventing increased mitochondria-derived reactive oxygen species (ROS) and subsequent cytochrome c release, caspase activation, and mitochondrial damage in nerve growth factor (NGF)-deprived sympathetic neurons, while MitoE2 was largely ineffective. In this paradigm, the most proximal point of divergence was the ability of MitoQ10 to scavenge mitochondrial superoxide (O2(-)). MitoQ10 also prevented caspase-independent neuronal death in these cells demonstrating that the mitochondrial redox state significantly influences both apoptotic and nonapoptotic pathways leading to neuronal death. We suggest that mitochondria-targeted antioxidants may provide tools for delineating the role and significance of mitochondrial ROS in neuronal death and provide a new therapeutic approach for neurodegenerative conditions involving trophic factor deficits and multiple modes of cell death.

Indexed as

ApoptosisAnimalsAntioxidantsCaspasesCells, CulturedFemaleMaleMiceMice, Inbred C57BLMitochondriaNerve Growth FactorsNeuronsOrganophosphorus CompoundsReactive Oxygen SpeciesUbiquinoneAntioxidantsCaspasesmitoquinoneNerve Growth FactorsOrganophosphorus CompoundsReactive Oxygen SpeciesUbiquinoneApoptosisCaspaseCytochrome cMitochondriaMitoQROS

Identifiers

PMID25239010
PMCPMC4250393
OpenAlexW2050392023

What OpenQuestion holds

Textmetadata
LicenceTDM
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.