Evidence map›Paper›PMID 22938055›Full record

ArticleAntioxidants & redox signaling2013

Is inflammation a mitochondrial dysfunction-dependent event in fibromyalgia?

Mario D Cordero, Eduardo Díaz-Parrado, Angel M Carrión, Simona Alfonsi, José Antonio Sánchez-Alcazar, Pedro Bullón, Maurizio Battino, Manuel de Miguel

Abstract read
In one paragraph

Article in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Effect of Coenzyme QCNS neuroscience & therapeutics · 2017
    Trial
  4. Trial
  5. Article
  6. Article
  7. Article
  8. Review
  9. Redox reactions in chronic pain: mechanisms and relevance in fibromyalgia.Frontiers in pain research (Lausanne, Switzerland) · 2025
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Bioactive Compounds for Fibromyalgia-like Symptoms: A Narrative Review and Future Perspectives.International journal of environmental research and public health · 2022
    Review
  18. Article
  19. Review
  20. 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

8 authors at 4 institutions in 2 countries.

Mario D CorderoDpto. Citología e Histología Normal y Patológica, Facultad de Medicina, Universidad de Sevilla, Spain. mdcormor@us.es
Eduardo Díaz-Parrado
Angel M Carrión
Simona Alfonsi
José Antonio Sánchez-Alcazar
Pedro Bullón
Maurizio Battino
Manuel de Miguel
Universidad de Sevilla · ESMarche Polytechnic University · ITCentro Andaluz de Biología del Desarrollo · ESUniversidad Pablo de Olavide · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibromyalgia (FM) is a complex disorder that affects up to 5% of the general population worldwide. Both mitochondrial dysfunction and inflammation have been implicated in the pathophysiology of FM. We have investigated the possible relationship between mitochondrial dysfunction, oxidative stress, and inflammation in FM. We studied 30 women diagnosed with FM and 20 healthy women. Blood mononuclear cells (BMCs) from FM patients showed reduced level of coenzyme Q₁₀ (CoQ₁₀) and mtDNA contents and high level of mitochondrial reactive oxygen species (ROS) and serum tumor necrosis factor (TNF)-alpha and transcript levels. A significant negative correlation between CoQ₁₀ and TNF-alpha levels (r=-0.588; p<0.01), and a positive correlation between ROS and TNF-alpha levels (r=0.791; p<0.001) were observed accompanied by a significant correlation of visual analogical scale with serum TNF-alpha and transcript levels (r=0.4507; p<0.05 and r=0.7089; p<0.001, respectively). TNF-alpha release was observed in an in vitro (BMCs) and in vivo (mice) CoQ₁₀ deficiency model. Oral CoQ₁₀ supplementation restored biochemical parameters and induced a significant improvement in clinical symptoms (p<0.001). These results lead to the hypothesis that inflammation could be a mitochondrial dysfunction-dependent event implicated in the pathophysiology of FM in several patients indicating at mitochondria as a possible new therapeutic target.

Indexed as

AnimalsDisease Models, AnimalFemaleFibromyalgiaHumansInflammationLeukocytes, MononuclearMaleMiceMitochondriaReactive Oxygen SpeciesTumor Necrosis Factor-alphaUbiquinonecoenzyme Q10Reactive Oxygen SpeciesTumor Necrosis Factor-alphaUbiquinone

Identifiers

PMID22938055
PMCPMC3555092
OpenAlexW2108435852

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.