Evidence map›Paper›PMID 37777633›Full record

ArticleScientific reports2023

A possible role for proinflammatory activation via cGAS-STING pathway in atherosclerosis induced by accumulation of DNA double-strand breaks.

Chiemi Sakai, Keitaro Ueda, Kohei Goda, Rikuto Fujita, Junji Maeda, Shinya Nakayama, Yusuke Sotomaru, Satoshi Tashiro, Masao Yoshizumi, Takafumi Ishida and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Aging-AssociatedJournal of the American Heart Association · 2026
    Article
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  11. Neutrophil Extracellular Traps in Atherosclerosis: Research Progress.International journal of molecular sciences · 2025
    Review
  12. The role of interferon regulatory factors in atherosclerosis.Frontiers in cardiovascular medicine · 2025
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
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 5 institutions in 1 country.

Chiemi SakaiDepartment of Cardiovascular Physiology and Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima, 734-8551, Japan.
Keitaro UedaDepartment of Cardiovascular Physiology and Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima, 734-8551, Japan.
Kohei GodaDepartment of Cardiovascular Physiology and Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima, 734-8551, Japan.
Rikuto FujitaNational Hospital Organization, Higashihiroshima Medical Center, Hiroshima City, Japan.
Junji MaedaDepartment of Cardiology, Tsuchiya General Hospital, Hiroshima City, Japan.
Shinya NakayamaDepartment of Cellular Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima City, Japan.
Yusuke SotomaruNatural Science Center for Basic Research and Development, Hiroshima University, Hiroshima City, Japan.
Satoshi TashiroDepartment of Cellular Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima City, Japan.
Masao YoshizumiDepartment of Cardiovascular Physiology and Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima, 734-8551, Japan.
Takafumi IshidaDepartment of Cardiovascular Medicine, Fukushima Medical University, Fukushima, Japan.
Mari IshidaDepartment of Cardiovascular Physiology and Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima, 734-8551, Japan. mari@hiroshima-u.ac.jp.
Hiroshima University · JPFukushima Medical University · JPHigashihiroshima Medical Center · JPHiroshima City University · JPHiroshima General Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA damage contributes to atherosclerosis. However, causative links between DNA double-strand breaks (DSBs) and atherosclerosis have yet to be established. Here, we investigated the role of DSBs in atherosclerosis using mice and vascular cells deficient in Ku80, a DSB repair protein. After 4 weeks of a high-fat diet, Ku80-deficient apolipoprotein E knockout mice (Ku80

Indexed as

AtherosclerosisDNA Breaks, Double-StrandedPlaque, AtheroscleroticAnimalsApolipoproteins ECyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseCytokinesDNAInterleukin-6MiceMice, KnockoutNucleotidyltransferasesSTING ProteinApolipoproteins EcGAS protein, mouseCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseCytokinesDNAInterleukin-6NucleotidyltransferasesSting1 protein, mouseSTING Protein

Identifiers

PMID37777633
PMCPMC10542807
OpenAlexW4387216516

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.