Evidence map›Paper›PMID 28511347›Full record

ArticleRedox biology2017

Mitochondrial complex I deactivation is related to superoxide production in acute hypoxia.

Pablo Hernansanz-Agustín, Elena Ramos, Elisa Navarro, Esther Parada, Nuria Sánchez-López, Laura Peláez-Aguado, J Daniel Cabrera-García, Daniel Tello, Izaskun Buendia, Anabel Marina and 4 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

74 citing papers in PubMed, 143 citations in OpenAlex.

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  12. Is Emerging Nanomedicine a Friend or Foe to Germ Cells?International journal of nanomedicine · 2025
    Review
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  14. Article
  15. Article
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  17. Revisiting reactive oxygen species production in hypoxia.Pflugers Archiv : European journal of physiology · 2024
    Review
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  19. Review
  20. Article

14 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

14 authors at 6 institutions in 2 countries.

Pablo Hernansanz-AgustínServicio de Inmunología, Hospital Universitario de La Princesa, Instituto de Investigación Sanitaria Princesa (IIS-IP), E-28006 Madrid, Spain; Departamento de Bioquímica, Facultad de Medicina, Universidad Autónoma de Madrid (UAM) and Instituto de Investigaciones Biomédicas Alberto Sols, E-28029 Madrid, Spain.
Elena RamosServicio de Inmunología, Hospital Universitario de La Princesa, Instituto de Investigación Sanitaria Princesa (IIS-IP), E-28006 Madrid, Spain.
Elisa NavarroInstituto Teófilo Hernando, Departamento de Farmacología y Terapéutica, Facultad de Medicina, Universidad Autónoma de Madrid (UAM), Instituto de Investigación Sanitaria Princesa (IIS-IP), E-28029 Madrid, Spain.
Esther ParadaInstituto Teófilo Hernando, Departamento de Farmacología y Terapéutica, Facultad de Medicina, Universidad Autónoma de Madrid (UAM), Instituto de Investigación Sanitaria Princesa (IIS-IP), E-28029 Madrid, Spain.
Nuria Sánchez-LópezServicio de Inmunología, Hospital Universitario de La Princesa, Instituto de Investigación Sanitaria Princesa (IIS-IP), E-28006 Madrid, Spain; Servicio de Proteómica, Centro de Biología Molecular "Severo Ochoa (CBSMO), Consejo Superior de Investigaciones Científicas (CSIC) - UAM, E-28049 Madrid, Spain.
Laura Peláez-AguadoServicio de Proteómica, Centro de Biología Molecular "Severo Ochoa (CBSMO), Consejo Superior de Investigaciones Científicas (CSIC) - UAM, E-28049 Madrid, Spain.
J Daniel Cabrera-GarcíaServicio de Inmunología, Hospital Universitario de La Princesa, Instituto de Investigación Sanitaria Princesa (IIS-IP), E-28006 Madrid, Spain.
Daniel TelloUnidad de Investigación, Hospital Santa Cristina, Universidad Autónoma de Madrid (UAM), Instituto de Investigación Sanitaria Princesa (IP), E-28009 Madrid, Spain.
Izaskun BuendiaInstituto Teófilo Hernando, Departamento de Farmacología y Terapéutica, Facultad de Medicina, Universidad Autónoma de Madrid (UAM), Instituto de Investigación Sanitaria Princesa (IIS-IP), E-28029 Madrid, Spain.
Anabel MarinaServicio de Proteómica, Centro de Biología Molecular "Severo Ochoa (CBSMO), Consejo Superior de Investigaciones Científicas (CSIC) - UAM, E-28049 Madrid, Spain.
Javier EgeaInstituto Teófilo Hernando, Departamento de Farmacología y Terapéutica, Facultad de Medicina, Universidad Autónoma de Madrid (UAM), Instituto de Investigación Sanitaria Princesa (IIS-IP), E-28029 Madrid, Spain.
Manuela G LópezInstituto Teófilo Hernando, Departamento de Farmacología y Terapéutica, Facultad de Medicina, Universidad Autónoma de Madrid (UAM), Instituto de Investigación Sanitaria Princesa (IIS-IP), E-28029 Madrid, Spain.
Anna BogdanovaInstitute of Veterinary Physiology, Vetsuisse Faculty and Zurich Center for Integrative Human Physiology (ZIHP), University of Zurich, CH-8057 Zurich, Switzerland.
Antonio Martínez-RuizServicio de Inmunología, Hospital Universitario de La Princesa, Instituto de Investigación Sanitaria Princesa (IIS-IP), E-28006 Madrid, Spain; Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Spain. Electronic address: amartinezruiz@salud.madrid.org.
Universidad Autónoma de Madrid · ESHospital Universitario de La Princesa · ESCentro de Biología Molecular Severo Ochoa · ESCentro de Investigación Biomédica en Red · ESConsejo Superior de Investigaciones Científicas · ESUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria use oxygen as the final acceptor of the respiratory chain, but its incomplete reduction can also produce reactive oxygen species (ROS), especially superoxide. Acute hypoxia produces a superoxide burst in different cell types, but the triggering mechanism is still unknown. Herein, we show that complex I is involved in this superoxide burst under acute hypoxia in endothelial cells. We have also studied the possible mechanisms by which complex I could be involved in this burst, discarding reverse electron transport in complex I and the implication of PTEN-induced putative kinase 1 (PINK1). We show that complex I transition from the active to 'deactive' form is enhanced by acute hypoxia in endothelial cells and brain tissue, and we suggest that it can trigger ROS production through its Na

Indexed as

AnimalsCattleCell HypoxiaCells, CulturedElectron Transport Complex IEndothelial CellsMitochondriaOxidation-ReductionProtein KinasesSignal TransductionSuperoxidesElectron Transport Complex IProtein KinasesSuperoxidesHypoxiaMitochondrial complex IOxygen sensingRedox signallingSuperoxide

Identifiers

PMID28511347
PMCPMC5430576
OpenAlexW2606455540

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.