Evidence map›Paper›PMID 31709317›Full record

ArticleJACC. Basic to translational science2019

Quantification of DNA Damage in Heart Tissue as a Novel Prediction Tool for Therapeutic Prognosis of Patients With Dilated Cardiomyopathy.

Toshiyuki Ko, Kanna Fujita, Seitaro Nomura, Yukari Uemura, Shintaro Yamada, Takashige Tobita, Manami Katoh, Masahiro Satoh, Masamichi Ito, Yukako Domoto and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JACC. Basic to translational science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.7field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. DNA damage and repair in cardiomyopathy: mechanisms and therapeutic opportunities.American journal of physiology. Heart and circulatory physiology · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 4 institutions in 1 country.

Toshiyuki KoDepartment of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Kanna FujitaDepartment of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Seitaro NomuraDepartment of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Yukari UemuraBiostatistics Division, Clinical Research Support Center, University of Tokyo Hospital, Tokyo, Japan.
Shintaro YamadaDepartment of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Takashige TobitaDepartment of Cardiology, Tokyo Women's Medical University, Tokyo, Japan.
Manami KatohGenome Science Division, Research Center for Advanced Science and Technology, University of Tokyo, Tokyo, Japan.
Masahiro SatohDepartment of Cardiovascular Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Masamichi ItoDepartment of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Yukako DomotoDepartment of Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Yumiko HosoyaDepartment of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Eisuke AmiyaDepartment of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Masaru HatanoDepartment of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Hiroyuki MoritaDepartment of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Masashi FukayamaDepartment of Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Hiroyuki AburataniGenome Science Division, Research Center for Advanced Science and Technology, University of Tokyo, Tokyo, Japan.
Issei KomuroDepartment of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
The University of Tokyo · JPChiba University · JPTokyo Women's Medical University · JPUniversity of Tokyo Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study evaluated myocardial nuclear staining for the DNA damage markers poly(ADP-ribose) (PAR) and γ-H2A.X in 58 patients with dilated cardiomyopathy. Patients with left ventricular reverse remodeling (LVRR) showed a significantly smaller proportion of PAR-positive nuclei and γ-H2A.X-positive nuclei in biopsy specimens compared with those without LVRR. Propensity analysis showed that the proportion of both PAR-positive and γ-H2A.X-positive nuclei were independent prognostic factors for LVRR. In conclusion, we showed the utility of DNA damage-marker staining to predict the probability of LVRR, thus revealing a novel prognostic predictor of medical therapy for dilated cardiomyopathy.

Indexed as

BMI, body mass indexBNP, B-type natriuretic peptideCI, confidence intervalDAPI, 4′,6-diamidino-2-phenylindoleDCM, dilated cardiomyopathydilated cardiomyopathyDNA damageIQR, interquartile rangeleft ventricular reverse remodelingLVAD, left ventricular assist deviceLVEF, left ventricular ejection fractionLVRR, left ventricular reverse remodelingNYHA, New York Heart AssociationPAR, poly(ADP-ribose)poly ADP-riboseROC, receiver-operating characteristicWGA, wheat germ agglutinin

Identifiers

PMID31709317
PMCPMC6834953
OpenAlexW2977002799

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.