Evidence map›Paper›PMID 33166073›Full record

ArticleAging cell2020

Cockayne syndrome proteins CSA and CSB maintain mitochondrial homeostasis through NAD

Mustafa N Okur, Evandro F Fang, Elayne M Fivenson, Vinod Tiwari, Deborah L Croteau, Vilhelm A Bohr

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Pharmacologic AMPK Activation Extends Lifespan inbioRxiv : the preprint server for biology · 2026
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Roles of NADCold Spring Harbor perspectives in medicine · 2024
    Review
  14. Article
  15. Article
  16. The mitophagy pathway and its implications in human diseases.Signal transduction and targeted therapy · 2023
    Review
  17. Article
  18. DNA Damage and Repair in Eye Diseases.International journal of molecular sciences · 2023
    Review
  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

6 authors at 2 institutions in 3 countries.

Mustafa N OkurLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.ORCID 0000-0001-5724-061X
Evandro F FangLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.ORCID 0000-0003-0355-7202
Elayne M FivensonLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.ORCID 0000-0001-6106-2588
Vinod TiwariLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.ORCID 0000-0003-2341-0953
Deborah L CroteauLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Vilhelm A BohrLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
National Institutes of Health · USUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cockayne syndrome (CS) is a rare premature aging disease, most commonly caused by mutations of the genes encoding the CSA or CSB proteins. CS patients display cachectic dwarfism and severe neurological manifestations and have an average life expectancy of 12 years. The CS proteins are involved in transcription and DNA repair, with the latter including transcription-coupled nucleotide excision repair (TC-NER). However, there is also evidence for mitochondrial dysfunction in CS, which likely contributes to the severe premature aging phenotype of this disease. While damaged mitochondria and impaired mitophagy were characterized in mice with CSB deficiency, such changes in the CS nematode model and CS patients are not fully known. Our cross-species transcriptomic analysis in CS postmortem brain tissue, CS mouse, and nematode models shows that mitochondrial dysfunction is indeed a common feature in CS. Restoration of mitochondrial dysfunction through NAD

Indexed as

Aging, PrematureAMP-Activated Protein KinasesAnimalsAnimals, Genetically ModifiedCaenorhabditis elegansCerebellumCockayne SyndromeDisease Models, AnimalDNA HelicasesDNA Repair EnzymesHumansLongevityMiceMice, Inbred C57BLMice, Mutant StrainsMitochondriaAMP-Activated Protein KinasesDNA HelicasesDNA Repair EnzymesERCC6 protein, humanERCC8 protein, humanNADPoly-ADP-Ribose Binding ProteinsTranscription Factorsaccelerated ageingagingAMPKCockayne syndromemitochondrial maintenancemitophagyNAD+

Identifiers

PMID33166073
PMCPMC7744955
OpenAlexW3103088161

What OpenQuestion holds

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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.