Evidence map›Paper›PMID 37627647›Full record

ReviewAntioxidants (Basel, Switzerland)2023

Primary Coenzyme Q10 Deficiency: An Update.

David Mantle, Lauren Millichap, Jesus Castro-Marrero, Iain P Hargreaves

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
6.0field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. CD8MedComm · 2026
    Review
  5. Article
  6. Article
  7. Bypass Treatments for Primary Coenzyme Q10 Deficiency: An Update.International journal of molecular sciences · 2026
    Review
  8. Review
  9. Review
  10. Mitochondrial Transplantation as a Therapeutic Strategy for Inherited Mitochondrial Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. HPDL Variant Type Correlates With Clinical Disease Onset and Severity.Annals of clinical and translational neurology · 2025
    Observational
  20. Coenzyme Q10 and Xenobiotic Metabolism: An Overview.International journal of molecular sciences · 2025
    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

4 authors at 3 institutions in 2 countries.

David MantlePharma Nord (UK) Ltd., Morpeth NE61 2DB, UK.
Lauren MillichapSchool of Pharmacy and Biomolecular Sciences, Liverpool John Moores University, Liverpool L3 3AF, UK.
Jesus Castro-MarreroRheumatology Research Group, ME/CFS Research Unit, Vall d'Hebron Research Institute, Universitat Autonoma de Barcelona, 08035 Barcelona, Spain.ORCID 0000-0002-2481-3052
Iain P HargreavesSchool of Pharmacy and Biomolecular Sciences, Liverpool John Moores University, Liverpool L3 3AF, UK.
Liverpool John Moores University · GBPharma Nord (United Kingdom) · GBUniversitat Autònoma de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coenzyme Q10 (CoQ10) has a number of vital functions in all cells, both mitochondrial and extra-mitochondrial. In addition to its key role in mitochondrial oxidative phosphorylation, CoQ10 serves as a lipid soluble antioxidant and plays an important role in fatty acid beta-oxidation and pyrimidine and lysosomal metabolism, as well as directly mediating the expression of a number of genes, including those involved in inflammation. Due to the multiplicity of roles in cell function, it is not surprising that a deficiency in CoQ10 has been implicated in the pathogenesis of a wide range of disorders. CoQ10 deficiency is broadly divided into primary and secondary types. Primary CoQ10 deficiency results from mutations in genes involved in the CoQ10 biosynthetic pathway. In man, at least 10 genes are required for the biosynthesis of functional CoQ10, a mutation in any one of which can result in a deficit in CoQ10 status. Patients may respond well to oral CoQ10 supplementation, although the condition must be recognised sufficiently early, before irreversible tissue damage has occurred. In this article, we have reviewed clinical studies (up to March 2023) relating to the identification of these deficiencies, and the therapeutic outcomes of CoQ10 supplementation; we have attempted to resolve the disparities between previous review articles regarding the usefulness or otherwise of CoQ10 supplementation in these disorders. In addition, we have highlighted several of the potential problems relating to CoQ10 supplementation in primary CoQ10 deficiency, as well as identifying unresolved issues relating to these disorders that require further research.

Indexed as

ataxiacardiomyopathyCoenzyme Q10encephalopathyprimary deficiencysteroid-resistant nephrotic syndrome

Identifiers

PMID37627647
PMCPMC10451954
OpenAlexW4386051163

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.