Evidence map›Paper›PMID 31160091›Full record

ArticleBiochemical and biophysical research communications2019

Ablation of Toll-like receptor 9 attenuates myocardial ischemia/reperfusion injury in mice.

Rika Kitazume-Taneike, Manabu Taneike, Shigemiki Omiya, Tomofumi Misaka, Kazuhiko Nishida, Osamu Yamaguchi, Shizuo Akira, Michael J Shattock, Yasushi Sakata, Kinya Otsu

Open access · hybridAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
4.5field-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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. NF-Frontiers in cardiovascular medicine · 2026
    Review
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  7. Article
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  9. Review
  10. Mitochondrial DNA signals driving immune responses: Why, How, Where?Cell communication and signaling : CCS · 2025
    Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Protection of CAPE-pNOInflammation · 2022
    Article
  20. 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

10 authors at 3 institutions in 2 countries.

Rika Kitazume-TaneikeThe School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Research Excellence, The James Black Centre, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom; Department of Cardiovascular Medicine, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Manabu TaneikeThe School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Research Excellence, The James Black Centre, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom; Department of Cardiovascular Medicine, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Shigemiki OmiyaThe School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Research Excellence, The James Black Centre, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom.
Tomofumi MisakaThe School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Research Excellence, The James Black Centre, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom.
Kazuhiko NishidaThe School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Research Excellence, The James Black Centre, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom.
Osamu YamaguchiDepartment of Cardiovascular Medicine, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Shizuo AkiraLaboratory of Host Defense, World Premier International Immunology Frontier Research Center, Osaka University, 2nd Fl. IFReC Research Building, 3-1 Yamadaoka, Suita, Osaka, 565-0871, Japan; Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Michael J ShattockThe School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Research Excellence, The James Black Centre, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom.
Yasushi SakataDepartment of Cardiovascular Medicine, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Kinya OtsuThe School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Research Excellence, The James Black Centre, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom. Electronic address: kinya.otsu@kcl.ac.uk.
Osaka University · JPBritish Heart Foundation · GBKing's College London · GB

Funding

British Heart Foundation CH/11/3/29051British Heart Foundation RG/11/12/29052British Heart Foundation RG/12/4/29426British Heart Foundation RG/16/15/32294
6 · The paper itself

Abstract

In myocardial ischemia/reperfusion injury, the innate immune and subsequent inflammatory responses play a crucial role in the extension of myocardial damage. Toll-like receptor 9 (TLR9) is a critical receptor for recognizing unmethylated CpG motifs that mitochondria contain in their DNA, and induces inflammatory responses. The aim of this study was to elucidate the role of TLR9 in myocardial ischemia/reperfusion injury. Isolated hearts from TLR9-deficient and control wild-type mice were subjected to 35 min of global ischemia, followed by 60 min of reperfusion with Langendorff apparatus. Furthermore, wild-type mouse hearts were infused with DNase I and subjected to ischemia/reperfusion. Ablation of TLR9-mediated signaling pathway attenuates myocardial ischemia/reperfusion injury and inflammatory responses, and digestion of extracellular mitochondrial DNA released from the infarct heart partially improved myocardial ischemia/reperfusion injury with no effect on inflammatory responses. TLR9 could be a therapeutic target to reduce myocardial ischemia/reperfusion injury.

Indexed as

AnimalsCytokinesDeoxyribonuclease IGene Expression RegulationHeart Function TestsInflammation MediatorsMice, Inbred C57BLMyocardial Reperfusion InjuryNecrosisRNA, MessengerToll-Like Receptor 9CytokinesDeoxyribonuclease IInflammation MediatorsRNA, MessengerToll-Like Receptor 9InflammationLangendorff-perfused mouse heartMitochondrial DNAMyocardial ischemia/reperfusion injuryToll-like receptor 9

Identifiers

PMID31160091
PMCPMC6590932
OpenAlexW2947945825

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.