Evidence map›Paper›PMID 34680574›Full record

ArticleBiomedicines2021

β-RA Targets Mitochondrial Metabolism and Adipogenesis, Leading to Therapeutic Benefits against CoQ Deficiency and Age-Related Overweight.

Agustín Hidalgo-Gutiérrez, Eliana Barriocanal-Casado, María Elena Díaz-Casado, Pilar González-García, Riccardo Zenezini Chiozzi, Darío Acuña-Castroviejo, Luis Carlos López

Open access · goldAbstract read
In one paragraph

Article in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 25% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. The efficacy of coenzyme QJournal of cellular and molecular medicine · 2022
    Pooled it
  2. Article
  3. Article
  4. Review
  5. Coenzyme QFree radical biology & medicine · 2025
    Article
  6. Article
  7. Understanding coenzyme Q.Physiological reviews · 2024
    Review
  8. Article
  9. Article
  10. A novelMolecular genetics and metabolism reports · 2022
    Article
  11. Review
  12. Article
  13. 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

7 authors at 2 institutions in 2 countries.

Agustín Hidalgo-GutiérrezDepartamento de Fisiología, Facultad de Medicina, Universidad de Granada, 18016 Granada, Spain.ORCID 0000-0001-6414-6859
Eliana Barriocanal-CasadoDepartamento de Fisiología, Facultad de Medicina, Universidad de Granada, 18016 Granada, Spain.
María Elena Díaz-CasadoDepartamento de Fisiología, Facultad de Medicina, Universidad de Granada, 18016 Granada, Spain.
Pilar González-GarcíaDepartamento de Fisiología, Facultad de Medicina, Universidad de Granada, 18016 Granada, Spain.ORCID 0000-0002-9560-2957
Riccardo Zenezini ChiozziBiomolecular Mass Spectrometry and Proteomics, Bijvoet Center for Biomolecular Research, Utrecht Institute for Pharmaceutical Sciences, University of Utrecht, Padualaan 8, 3584 CH Utrecht, The Netherlands.
Darío Acuña-CastroviejoDepartamento de Fisiología, Facultad de Medicina, Universidad de Granada, 18016 Granada, Spain.ORCID 0000-0002-9680-1560
Luis Carlos LópezDepartamento de Fisiología, Facultad de Medicina, Universidad de Granada, 18016 Granada, Spain.ORCID 0000-0003-3355-0298
Universidad de Granada · ESUtrecht University · NL

Funding

European Union 823839Ministerio de Ciencia e Innovacion RTI2018-093503-B-100Muscular Dystrophy Association MDA-602322Regional Government of Andalusia P20_00134
6 · The paper itself

Abstract

Primary mitochondrial diseases are caused by mutations in mitochondrial or nuclear genes, leading to the abnormal function of specific mitochondrial pathways. Mitochondrial dysfunction is also a secondary event in more common pathophysiological conditions, such as obesity and metabolic syndrome. In both cases, the improvement and management of mitochondrial homeostasis remain challenging. Here, we show that beta-resorcylic acid (β-RA), which is a natural phenolic compound, competed in vivo with 4-hydroxybenzoic acid, which is the natural precursor of coenzyme Q biosynthesis. This led to a decrease in demethoxyubiquinone, which is an intermediate metabolite of CoQ biosynthesis that is abnormally accumulated in

Indexed as

3T3-L1astrogliosisencephalopathyhepatic steatosismitochondrial diseasemitochondrial proteomemouse modelobesityspongiosiswhite adipose tissue

Identifiers

PMID34680574
PMCPMC8533582
OpenAlexW3207357383

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.