Evidence map›Paper›PMID 25272163›Full record

ArticlePloS one2014

Coenzyme Q10 protects human endothelial cells from β-amyloid uptake and oxidative stress-induced injury.

Mario Durán-Prado, Javier Frontiñán, Raquel Santiago-Mora, Juan Ramón Peinado, Cristina Parrado-Fernández, María Victoria Gómez-Almagro, María Moreno, José Alberto López-Domínguez, José Manuel Villalba, Francisco J Alcaín

Abstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

36 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. The cellular model for Alzheimer's disease research: PC12 cells.Frontiers in molecular neuroscience · 2022
    Pooled it
  2. Salvage of the retinal ganglion cells in transition phase in Alzheimer's disease with topical coenzyme Q10: is it possible?Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2020
    Trial
  3. Trial
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. CoQAntioxidants (Basel, Switzerland) · 2024
    Review
  10. Review
  11. New Insights on the Uptake and Trafficking of Coenzyme Q.Antioxidants (Basel, Switzerland) · 2023
    Review
  12. Coenzyme Q10 and Dementia: A Systematic Review.Antioxidants (Basel, Switzerland) · 2023
    Review
  13. Review
  14. Article
  15. Article
  16. Coenzyme Q10, Ageing and the Nervous System: An Overview.Antioxidants (Basel, Switzerland) · 2021
    Review
  17. Article
  18. Article
  19. Role of Coenzyme QAntioxidants (Basel, Switzerland) · 2021
    Review
  20. The Use of Coenzyme Q10 in Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2021
    Review
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

10 authors.

Mario Durán-PradoDepartment of Medical Sciences, Faculty of Medicine, University of Castilla-la Mancha, Ciudad Real, Spain; Oxidative Stress and Neurodegeneration Group, Regional Centre for Biomedical Research, Ciudad Real, Spain.
Javier FrontiñánDepartment of Medical Sciences, Faculty of Medicine, University of Castilla-la Mancha, Ciudad Real, Spain; Oxidative Stress and Neurodegeneration Group, Regional Centre for Biomedical Research, Ciudad Real, Spain.
Raquel Santiago-MoraDepartment of Medical Sciences, Faculty of Medicine, University of Castilla-la Mancha, Ciudad Real, Spain.
Juan Ramón PeinadoDepartment of Medical Sciences, Faculty of Medicine, University of Castilla-la Mancha, Ciudad Real, Spain; Oxidative Stress and Neurodegeneration Group, Regional Centre for Biomedical Research, Ciudad Real, Spain.
Cristina Parrado-FernándezDepartment of Medical Sciences, Faculty of Medicine, University of Castilla-la Mancha, Ciudad Real, Spain; Oxidative Stress and Neurodegeneration Group, Regional Centre for Biomedical Research, Ciudad Real, Spain.
María Victoria Gómez-AlmagroDepartment of Organic Chemistry, Faculty of Chemical Sciences and Technologies and Instituto Regional de Investigación Científica Aplicada, Universidad de Castilla-La Mancha, Ciudad Real, Spain; Fundación Parque Científico y Tecnológico de Albacete, Albacete, Spain.
María MorenoDepartment of Organic Chemistry, Faculty of Chemical Sciences and Technologies and Instituto Regional de Investigación Científica Aplicada, Universidad de Castilla-La Mancha, Ciudad Real, Spain.
José Alberto López-DomínguezDepartment of Cell Biology, Physiology and Immunology, Faculty of Sciences, University of Córdoba, Agrifood Campus of International Excellence ceiA3, Córdoba, Spain.
José Manuel VillalbaDepartment of Cell Biology, Physiology and Immunology, Faculty of Sciences, University of Córdoba, Agrifood Campus of International Excellence ceiA3, Córdoba, Spain.
Francisco J AlcaínDepartment of Medical Sciences, Faculty of Medicine, University of Castilla-la Mancha, Ciudad Real, Spain; Oxidative Stress and Neurodegeneration Group, Regional Centre for Biomedical Research, Ciudad Real, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuropathological symptoms of Alzheimer's disease appear in advances stages, once neuronal damage arises. Nevertheless, recent studies demonstrate that in early asymptomatic stages, ß-amyloid peptide damages the cerebral microvasculature through mechanisms that involve an increase in reactive oxygen species and calcium, which induces necrosis and apoptosis of endothelial cells, leading to cerebrovascular dysfunction. The goal of our work is to study the potential preventive effect of the lipophilic antioxidant coenzyme Q (CoQ) against ß-amyloid-induced damage on human endothelial cells. We analyzed the protective effect of CoQ against Aβ-induced injury in human umbilical vein endothelial cells (HUVECs) using fluorescence and confocal microscopy, biochemical techniques and RMN-based metabolomics. Our results show that CoQ pretreatment of HUVECs delayed Aβ incorporation into the plasma membrane and mitochondria. Moreover, CoQ reduced the influx of extracellular Ca(2+), and Ca(2+) release from mitochondria due to opening the mitochondrial transition pore after β-amyloid administration, in addition to decreasing O2(.-) and H2O2 levels. Pretreatment with CoQ also prevented ß-amyloid-induced HUVECs necrosis and apoptosis, restored their ability to proliferate, migrate and form tube-like structures in vitro, which is mirrored by a restoration of the cell metabolic profile to control levels. CoQ protected endothelial cells from Aβ-induced injury at physiological concentrations in human plasma after oral CoQ supplementation and thus could be a promising molecule to protect endothelial cells against amyloid angiopathy.

Indexed as

Oxidative StressAmyloid beta-PeptidesEndothelium, VascularHumansHuman Umbilical Vein Endothelial CellsUbiquinoneAmyloid beta-Peptidescoenzyme Q10Ubiquinone

Identifiers

PMID25272163
PMCPMC4182835

What OpenQuestion holds

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LicenceCC BY
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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.