Evidence map›Paper›PMID 31115493›Full record

ArticleInternational journal of molecular medicine2019

Mitochondrial electron transport chain, ROS generation and uncoupling (Review).

Ru-Zhou Zhao, Shuai Jiang, Lin Zhang, Zhi-Bin Yu

Open access · bronzeAbstract read
In one paragraph

Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 952 papers.

0numbers the graph read from it
0cells of the map it votes in
952citing papers in PubMed
76.2field-weighted citation impact, top 1% 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

952 citing papers in PubMed, 1,365 citations in OpenAlex.

  1. Review
  2. PROTACs in cancer therapy: targeted degradation of GPX4, PARP and epigenetic regulators.Journal of enzyme inhibition and medicinal chemistry · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

892 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 at 1 institution in 1 country.

Ru-Zhou ZhaoDepartment of Aerospace Physiology, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China.
Shuai JiangDepartment of Aerospace Physiology, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China.
Lin ZhangDepartment of Aerospace Physiology, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China.
Zhi-Bin YuDepartment of Aerospace Physiology, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China.
Air Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mammalian mitochondrial electron transport chain (ETC) includes complexes I‑IV, as well as the electron transporters ubiquinone and cytochrome c. There are two electron transport pathways in the ETC: Complex I/III/IV, with NADH as the substrate and complex II/III/IV, with succinic acid as the substrate. The electron flow is coupled with the generation of a proton gradient across the inner membrane and the energy accumulated in the proton gradient is used by complex V (ATP synthase) to produce ATP. The first part of this review briefly introduces the structure and function of complexes I‑IV and ATP synthase, including the specific electron transfer process in each complex. Some electrons are directly transferred to O2 to generate reactive oxygen species (ROS) in the ETC. The second part of this review discusses the sites of ROS generation in each ETC complex, including sites IF and IQ in complex I, site IIF in complex II and site IIIQo in complex III, and the physiological and pathological regulation of ROS. As signaling molecules, ROS play an important role in cell proliferation, hypoxia adaptation and cell fate determination, but excessive ROS can cause irreversible cell damage and even cell death. The occurrence and development of a number of diseases are closely related to ROS overproduction. Finally, proton leak and uncoupling proteins (UCPS) are discussed. Proton leak consists of basal proton leak and induced proton leak. Induced proton leak is precisely regulated and induced by UCPs. A total of five UCPs (UCP1‑5) have been identified in mammalian cells. UCP1 mainly plays a role in the maintenance of body temperature in a cold environment through non‑shivering thermogenesis. The core role of UCP2‑5 is to reduce oxidative stress under certain conditions, therefore exerting cytoprotective effects. All diseases involving oxidative stress are associated with UCPs.

Indexed as

Oxidative StressSignal TransductionThermogenesisAnimalsCell HypoxiaCell ProliferationElectron Transport Chain Complex ProteinsHumansMitochondriaMitochondrial Uncoupling ProteinsReactive Oxygen SpeciesElectron Transport Chain Complex ProteinsMitochondrial Uncoupling ProteinsReactive Oxygen Species

Identifiers

PMID31115493
PMCPMC6559295
OpenAlexW2944315478

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.