Evidence map›Paper›PMID 27810734›Full record

ArticleRedox biology2016

The mitochondria-targeted antioxidant MitoQ modulates oxidative stress, inflammation and leukocyte-endothelium interactions in leukocytes isolated from type 2 diabetic patients.

Irene Escribano-Lopez, Noelia Diaz-Morales, Susana Rovira-Llopis, Arantxa Martinez de Marañon, Samuel Orden, Angeles Alvarez, Celia Bañuls, Milagros Rocha, Michael P Murphy, Antonio Hernandez-Mijares and 1 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 4% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Guidelines for evaluating endothelial function in vascular tissue.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Mitochondrial Dysfunction in the Cardio-Renal Axis.International journal of molecular sciences · 2023
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. 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

11 authors at 5 institutions in 2 countries.

Irene Escribano-LopezService of Endocrinology, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.
Noelia Diaz-MoralesService of Endocrinology, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.
Susana Rovira-LlopisService of Endocrinology, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain; Institute of Health Research INCLIVA, University of Valencia, Valencia, Spain.
Arantxa Martinez de MarañonService of Endocrinology, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.
Samuel OrdenCIBERehd - Department of Pharmacology and Physiology, University of Valencia, Valencia, Spain.
Angeles AlvarezCIBERehd - Department of Pharmacology and Physiology, University of Valencia, Valencia, Spain.
Celia BañulsService of Endocrinology, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain; Institute of Health Research INCLIVA, University of Valencia, Valencia, Spain.
Milagros RochaService of Endocrinology, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain; Institute of Health Research INCLIVA, University of Valencia, Valencia, Spain; CIBERehd - Department of Pharmacology and Physiology, University of Valencia, Valencia, Spain.
Michael P MurphyMRC Mitochondrial Biology Unit, Cambridge, United Kingdom.
Antonio Hernandez-MijaresService of Endocrinology, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain; Institute of Health Research INCLIVA, University of Valencia, Valencia, Spain; Department of Medicine, University of Valencia, Valencia, Spain.
Victor M VictorService of Endocrinology, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain; Institute of Health Research INCLIVA, University of Valencia, Valencia, Spain; CIBERehd - Department of Pharmacology and Physiology, University of Valencia, Valencia, Spain; Department of Physiology, University of Valencia, Valencia, Spain. Electronic address: victor.victor@uv.es.
Hospital Universitario Doctor Peset · ESUniversitat de València · ESFundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunitat Valenciana · ESINCLIVA Health Research Institute · ESMRC Mitochondrial Biology Unit · GB

Funding

Medical Research Council MC_U105663142
6 · The paper itself

Abstract

It is not known if the mitochondria-targeted antioxidants such as mitoquinone (MitoQ) can modulate oxidative stress and leukocyte-endothelium interactions in T2D patients. We aimed to evaluate the beneficial effect of MitoQ on oxidative stress parameters and leukocyte-endothelium interactions in leukocytes of T2D patients. The study population consisted of 98 T2D patients and 71 control subjects. We assessed metabolic and anthropometric parameters, mitochondrial reactive oxygen species (ROS) production, glutathione peroxidase 1 (GPX-1), NFκB-p65, TNFα and leukocyte-endothelium interactions. Diabetic patients exhibited higher weight, BMI, waist circumference, SBP, DBP, glucose, insulin, HOMA-IR, HbA1c, triglycerides, hs-CRP and lower HDL-c with respect to controls. Mitochondrial ROS production was enhanced in T2D patients and decreased by MitoQ. The antioxidant also increased GPX-1 levels and PMN rolling velocity and decreased PMN rolling flux and PMN adhesion in T2D patients. NFκB-p65 and TNFα were augmented in T2D and were both reduced by MitoQ treatment. Our findings support that the antioxidant MitoQ has an anti-inflammatory and antioxidant action in the leukocytes of T2D patients by decreasing ROS production, leukocyte-endothelium interactions and TNFα through the action of NFκB. These data suggest that mitochondria-targeted antioxidants such as MitoQ should be investigated as a novel means of preventing cardiovascular events in T2D patients.

Indexed as

AgedAnthropometryAnti-Inflammatory AgentsAntioxidantsDiabetes Mellitus, Type 2FemaleGlutathione PeroxidaseGlutathione Peroxidase GPX1HumansLeukocytesMaleMiddle AgedOrganophosphorus CompoundsOxidative StressReactive Oxygen SpeciesTranscription Factor RelAAnti-Inflammatory AgentsAntioxidantsGlutathione PeroxidaseGlutathione Peroxidase GPX1GPX1 protein, humanmitoquinoneOrganophosphorus CompoundsReactive Oxygen SpeciesRELA protein, humanTNF protein, humanTranscription Factor RelATumor Necrosis Factor-alphaUbiquinoneEndotheliumInflammationLeukocytesMitoQOxidative stressType 2 diabetes

Identifiers

PMID27810734
PMCPMC5094376
OpenAlexW2546238167

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.