Evidence map›Paper›PMID 34628368›Full record

ArticleAging2021

Neurovascular dysfunction and neuroinflammation in a Cockayne syndrome mouse model.

Gustavo Satoru Kajitani, Lear Brace, Jose Humberto Trevino-Villarreal, Kaspar Trocha, Michael Robert MacArthur, Sarah Vose, Dorathy Vargas, Roderick Bronson, Sarah Jayne Mitchell, Carlos Frederico Martins Menck and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Microglia-derived extracellular vesicles trigger age-related neurodegeneration upon DNA damage.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. DNA damage and repair in age-related inflammation.Nature reviews. Immunology · 2023
    Review
  11. Review
  12. 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

11 authors at 3 institutions in 3 countries.

Gustavo Satoru KajitaniDepartment of Genetics and Complex Diseases, Harvard School of Public Health, Boston, MA 02115, USA.
Lear BraceDepartment of Genetics and Complex Diseases, Harvard School of Public Health, Boston, MA 02115, USA.
Jose Humberto Trevino-VillarrealDepartment of Genetics and Complex Diseases, Harvard School of Public Health, Boston, MA 02115, USA.
Kaspar TrochaDepartment of Genetics and Complex Diseases, Harvard School of Public Health, Boston, MA 02115, USA.
Michael Robert MacArthurDepartment of Genetics and Complex Diseases, Harvard School of Public Health, Boston, MA 02115, USA.
Sarah VoseDepartment of Genetics and Complex Diseases, Harvard School of Public Health, Boston, MA 02115, USA.
Dorathy VargasRodent Histopathology Core, Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.
Roderick BronsonRodent Histopathology Core, Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.
Sarah Jayne MitchellDepartment of Genetics and Complex Diseases, Harvard School of Public Health, Boston, MA 02115, USA.
Carlos Frederico Martins MenckDepartamento de Microbiologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil.
James Robert MitchellDepartment of Genetics and Complex Diseases, Harvard School of Public Health, Boston, MA 02115, USA.
Harvard University · USETH Zurich · CHUniversidade de São Paulo · BR

Funding

VectorP30CA006516 · NCI · DANA-FARBER CANCER INSTITUTE · PI JENNIFER W MACK · 1985 to 2026
$330.6M
NCI NIH HHS P30 CA006516
6 · The paper itself

Abstract

Cockayne syndrome (CS) is a rare, autosomal genetic disorder characterized by premature aging-like features, such as cachectic dwarfism, retinal atrophy, and progressive neurodegeneration. The molecular defect in CS lies in genes associated with the transcription-coupled branch of the nucleotide excision DNA repair (NER) pathway, though it is not yet clear how DNA repair deficiency leads to the multiorgan dysfunction symptoms of CS. In this work, we used a mouse model of severe CS with complete loss of NER (

Indexed as

Disease Models, AnimalAgingAnimalsBlood-Brain BarrierBrainCockayne SyndromeDNA-Binding ProteinsDNA DamageDNA RepairEndothelial CellsMiceMice, KnockoutNeurogliaNeuroinflammatory DiseasesXeroderma Pigmentosum Group A ProteinCkn1 protein, mouseDNA-Binding ProteinsXeroderma Pigmentosum Group A ProteinXpa protein, mouseCockayne syndromeCSAinflammationsegmental progeriavascular dysfunctionXPA

Identifiers

PMID34628368
PMCPMC8544306
OpenAlexW3205671519

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.