Evidence map›Paper›PMID 28436431›Full record

ArticleNature communications2017

DNA single-strand break-induced DNA damage response causes heart failure.

Tomoaki Higo, Atsuhiko T Naito, Tomokazu Sumida, Masato Shibamoto, Katsuki Okada, Seitaro Nomura, Akito Nakagawa, Toshihiro Yamaguchi, Taku Sakai, Akihito Hashimoto and 9 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 135 citations in OpenAlex.

  1. Pooled it
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  5. Review
  6. DNA damage and repair in cardiomyopathy: mechanisms and therapeutic opportunities.American journal of physiology. Heart and circulatory physiology · 2026
    Review
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7 more citing papers are in PubMed but not listed here.

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

19 authors at 3 institutions in 2 countries.

Tomoaki HigoDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita 565-0871, Japan.
Atsuhiko T NaitoDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita 565-0871, Japan.
Tomokazu SumidaCREST, Sanbanmachi-building, 5 Sanbanmachi, Tokyo 102-0075, Japan.
Masato ShibamotoDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita 565-0871, Japan.
Katsuki OkadaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita 565-0871, Japan.
Seitaro NomuraCREST, Sanbanmachi-building, 5 Sanbanmachi, Tokyo 102-0075, Japan.
Akito NakagawaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita 565-0871, Japan.
Toshihiro YamaguchiDepartment of Cardiovascular Medicine, The University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Tokyo 113-8655, Japan.
Taku SakaiDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita 565-0871, Japan.
Akihito HashimotoDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita 565-0871, Japan.
Yuki KuramotoDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita 565-0871, Japan.
Masamichi ItoDepartment of Cardiovascular Medicine, The University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Tokyo 113-8655, Japan.
Shungo HikosoDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita 565-0871, Japan.
Hiroshi AkazawaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita 565-0871, Japan.
Jong-Kook LeeDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita 565-0871, Japan.
Ichiro ShiojimaCREST, Sanbanmachi-building, 5 Sanbanmachi, Tokyo 102-0075, Japan.
Peter J McKinnonDepartment of Genetics and Tumor Cell Biology, ST. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, Tennessee 38105, USA.
Yasushi SakataDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita 565-0871, Japan.
Issei KomuroCREST, Sanbanmachi-building, 5 Sanbanmachi, Tokyo 102-0075, Japan.
Osaka University · JPThe University of Tokyo · JPSt. Jude Children's Research Hospital · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
The DNA Damage Response and Tumorigenesis in the BrainP01CA096832 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI BAKER, SUZANNE J. · 2003 to 2025
$38.0M
ATM and DNA Damage in the Nervous SystemR01NS037956 · NINDS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI MCKINNON, PETER J · 1998 to 2022
$7.6M
ATM and DNA Damage in the Nervous SystemR56NS037956 · NINDS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI MCKINNON, PETER J · 2007 to 2007
$413k
NCI NIH HHS P01 CA096832NCI NIH HHS P30 CA021765NINDS NIH HHS R01 NS037956NINDS NIH HHS R56 NS037956
6 · The paper itself

Abstract

The DNA damage response (DDR) plays a pivotal role in maintaining genome integrity. DNA damage and DDR activation are observed in the failing heart, however, the type of DNA damage and its role in the pathogenesis of heart failure remain elusive. Here we show the critical role of DNA single-strand break (SSB) in the pathogenesis of pressure overload-induced heart failure. Accumulation of unrepaired SSB is observed in cardiomyocytes of the failing heart. Unrepaired SSB activates DDR and increases the expression of inflammatory cytokines through NF-κB signalling. Pressure overload-induced heart failure is more severe in the mice lacking XRCC1, an essential protein for SSB repair, which is rescued by blocking DDR activation through genetic deletion of ATM, suggesting the causative role of SSB accumulation and DDR activation in the pathogenesis of heart failure. Prevention of SSB accumulation or persistent DDR activation may become a new therapeutic strategy against heart failure.

Indexed as

DNA Breaks, Single-StrandedAnimalsAtaxia Telangiectasia Mutated ProteinsCytokinesDNADNA DamageDNA RepairGene Knockout TechniquesHeart FailureInflammationMiceMyocytes, CardiacNF-kappa BX-ray Repair Cross Complementing Protein 1Ataxia Telangiectasia Mutated ProteinsAtm protein, mouseCytokinesDNANF-kappa BX-ray Repair Cross Complementing Protein 1Xrcc1 protein, mouse

Identifiers

PMID28436431
PMCPMC5413978
OpenAlexW2607987923

What OpenQuestion holds

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Registered trials

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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.