Evidence map›Paper›PMID 22419586›Full record

ReviewBioFactors (Oxford, England)

Mitochondrial pharmacology: electron transport chain bypass as strategies to treat mitochondrial dysfunction.

Hani Atamna, Jeanette Mackey, Joseph M Dhahbi

Abstract readReview
In one paragraph

Review in BioFactors (Oxford, England). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

32 citing papers in PubMed, 60 citations in OpenAlex.

  1. Trial
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  9. Toluidine blue O directly and photodynamically impairs the bioenergetics of liver mitochondria: a potential mechanism of hepatotoxicity.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2023
    Article
  10. Review
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  13. Novel Therapeutic Approaches Against Acetaminophen-induced Liver Injury and Acute Liver Failure.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Resveratrol and Brain Mitochondria: a Review.Molecular neurobiology · 2018
    Review
  19. Carnosic Acid Suppresses the HMolecular 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 2 institutions in 1 country.

Hani AtamnaDepartment of Basic Sciences, Neuroscience, The Commonwealth Medical College, Scranton, PA 18509, USA. hatamna@tcmedc.org
Jeanette Mackey
Joseph M Dhahbi
Commonwealth Medical College · USUniversity of California, Riverside · US

Funding

Understanding the mechanism of cell senescence delay by methylene blueR15AG041414 · NIA · GEISINGER COMMONWEALTH SCHOOL OF MEDICINE · PI ATAMNA, HANI · 2011 to 2011
$314k
NIA NIH HHS R15 AG041414NIA NIH HHS R15AG041414
6 · The paper itself

Abstract

Mitochondrial dysfunction (primary or secondary) is detrimental to intermediary metabolism. Therapeutic strategies to treat/prevent mitochondrial dysfunction could be valuable for managing metabolic and age-related disorders. Here, we review strategies proposed to treat mitochondrial impairment. We then concentrate on redox-active agents, with mild-redox potential, who shuttle electrons among specific cytosolic or mitochondrial redox-centers. We propose that specific redox agents with mild redox potential (-0.1 V; 0.1 V) improve mitochondrial function because they can readily donate or accept electrons in biological systems, thus they enhance metabolic activity and prevent reactive oxygen species (ROS) production. These agents are likely to lack toxic effects because they lack the risk of inhibiting electron transfer in redox centers. This is different from redox agents with strong negative (-0.4 V; -0.2 V) or positive (0.2 V; 0.4 V) redox potentials who alter the redox status of redox-centers (i.e., become permanently reduced or oxidized). This view has been demonstrated by testing the effect of several redox active agents on cellular senescence. Methylene blue (MB, redox potential ≅10 mV) appears to readily cycle between the oxidized and reduced forms using specific mitochondrial and cytosolic redox centers. MB is most effective in delaying cell senescence and enhancing mitochondrial function in vivo and in vitro. Mild-redox agents can alter the biochemical activity of specific mitochondrial components, which then in response alters the expression of nuclear and mitochondrial genes. We present the concept of mitochondrial electron-carrier bypass as a potential result of mild-redox agents, a method to prevent ROS production, improve mitochondrial function, and delay cellular aging. Thus, mild-redox agents may prevent/delay mitochondria-driven disorders.

Indexed as

AnimalsElectron TransportHumansMethylene BlueMitochondriaOxidation-ReductionMethylene Blue

Identifiers

PMID22419586
PMCPMC4299858
OpenAlexW2022827665

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.