Evidence map›Paper›PMID 28121478›Full record

ArticleAutophagy2017

MitoQ regulates autophagy by inducing a pseudo-mitochondrial membrane potential.

Chao Sun, Xiongxiong Liu, Cuixia Di, Zhenhua Wang, Xiangquan Mi, Yang Liu, Qiuyue Zhao, Aihong Mao, Weiqiang Chen, Lu Gan and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.3field-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

39 citing papers in PubMed, 77 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
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  8. Non-pathogenic Trojan horseMaterials today. Bio · 2024
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  12. Systems-level analyses dissociate genetic regulators of reactive oxygen species and energy production.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 1 country.

Chao Suna Institute of Modern Physics, Chinese Academy of Sciences , Lanzhou , China.
Xiongxiong Liua Institute of Modern Physics, Chinese Academy of Sciences , Lanzhou , China.
Cuixia Dia Institute of Modern Physics, Chinese Academy of Sciences , Lanzhou , China.
Zhenhua Wangd College of Life Sciences , Yantai University , Yantai , China.
Xiangquan Mie College of Life Sciences , Lanzhou University , Lanzhou , China.
Yang Liua Institute of Modern Physics, Chinese Academy of Sciences , Lanzhou , China.
Qiuyue Zhaoa Institute of Modern Physics, Chinese Academy of Sciences , Lanzhou , China.
Aihong Maoa Institute of Modern Physics, Chinese Academy of Sciences , Lanzhou , China.
Weiqiang Chena Institute of Modern Physics, Chinese Academy of Sciences , Lanzhou , China.
Lu Gana Institute of Modern Physics, Chinese Academy of Sciences , Lanzhou , China.
Hong Zhanga Institute of Modern Physics, Chinese Academy of Sciences , Lanzhou , China.
Chinese Academy of Sciences · CNInstitute of Modern Physics · CNLanzhou University · CNYantai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During the process of oxidative phosphorylation, protons are pumped into the mitochondrial intermembrane space to establish a mitochondrial membrane potential (MMP). The electrochemical gradient generated allows protons to return to the matrix through the ATP synthase complex and generates ATP in the process. MitoQ is a lipophilic cationic drug that is adsorbed to the inner mitochondrial membrane; however, the cationic moiety of MitoQ remains in the intermembrane space. We found that the positive charges in MitoQ inhibited the activity of respiratory chain complexes I, III, and IV, reduced proton production, and decreased oxygen consumption. Therefore, a pseudo-MMP (PMMP) was formed via maintenance of exogenous positive charges. Proton backflow was severely impaired, leading to a decrease in ATP production and an increase in AMP production. Excess AMP activates AMP kinase, which inhibits the MTOR (mechanistic target of rapamycin) pathway and induces macroautophagy/autophagy. Therefore, we conclude that MitoQ increases PMMP via proton displacement with exogenous positive charges. In addition, PMMP triggered autophagy in hepatocellular carcinoma HepG2 cells via modification of mitochondrial bioenergetics pathways.

Indexed as

Adenylate KinaseAutophagyCell ProliferationEnergy MetabolismHep G2 CellsHumansMembrane Potential, MitochondrialMitochondriaOrganophosphorus CompoundsSignal TransductionTOR Serine-Threonine KinasesUbiquinoneAdenylate KinasemitoquinoneOrganophosphorus CompoundsTOR Serine-Threonine KinasesUbiquinoneautophagyenergy metabolismMitoQproton displacementpseudo-MMP

Identifiers

PMID28121478
PMCPMC5388232
OpenAlexW2582092041

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.