Evidence map›Paper›PMID 30423020›Full record

ArticleCardiovascular research2019

Targeted expression of cyclin D2 ameliorates late stage anthracycline cardiotoxicity.

Wuqiang Zhu, Sean Reuter, Loren J Field

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed, 31 citations in OpenAlex.

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  17. Cell Cycle Proteins as Key Regulators of Postmitotic Cell Death.The Yale journal of biology and medicine · 2019
    Review
  18. Small animal models of heart failure.Cardiovascular research · 2019
    Review
  19. Review
  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

3 authors at 2 institutions in 1 country.

Wuqiang ZhuThe Krannert Institute of Cardiology and the Wells Center for Pediatric Research, Indiana University School of Medicine, 1044 West Walnut Street, R4 Building Room W376, Indianapolis, IN, USA.
Sean ReuterThe Krannert Institute of Cardiology and the Wells Center for Pediatric Research, Indiana University School of Medicine, 1044 West Walnut Street, R4 Building Room W376, Indianapolis, IN, USA.
Loren J FieldThe Krannert Institute of Cardiology and the Wells Center for Pediatric Research, Indiana University School of Medicine, 1044 West Walnut Street, R4 Building Room W376, Indianapolis, IN, USA.
Indiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

Cardiomyocyte cell cycle activity in injured heartsR01HL132927 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI FIELD, LOREN J · 2017 to 2020
$1.6M
Myocardial Repair with a Novel Engineered Cardiac Muscle PatchR56HL142627 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ZHU, WUQIANG · 2018 to 2018
$371k
NHLBI NIH HHS R01 HL132927NHLBI NIH HHS R56 HL142627
6 · The paper itself

Abstract

aimsDoxorubicin (DOX) is a widely used and effective anti-cancer therapeutic. DOX treatment is associated with both acute and late onset cardiotoxicity, limiting its overall efficacy. Here, the impact of cardiomyocyte cell cycle activation was examined in a juvenile model featuring aspects of acute and late onset DOX cardiotoxicity. METHODS AND

resultsTwo-week old MHC-cycD2 transgenic mice (which express cyclin D2 in postnatal cardiomyocytes and exhibit sustained cardiomyocyte cell cycle activity; D2 mice) and their wild type (WT) littermates received weekly DOX injections for 5 weeks (25 mg/kg cumulative dose). One week after the last DOX treatment (acute stage), cardiac function was suppressed in both groups. Acute DOX cardiotoxicity in D2 and WT mice was associated with similar increases in the levels of cardiomyocyte apoptosis and Ku70/Ku80 expression (markers of DNA damage and oxidative stress), as well as similar reductions in hypertrophic cardiomyocyte growth. Cardiac dysfunction persisted in WT mice for 13 weeks following the last DOX treatment (late stage) and was accompanied by increased levels of cardiomyocyte apoptosis, Ku expression, and myocardial fibrosis. In contrast, D2 mice exhibited a progressive recovery in cardiac function, which was indistinguishable from saline-treated animals by 9 weeks following the last DOX treatment. Improved cardiac function was accompanied by reductions in the levels of late stage cardiomyocyte apoptosis, Ku expression, and myocardial fibrosis.

conclusionThese data suggest that cardiomyocyte cell cycle activity can promote recovery of cardiac function and preserve cardiac structure following DOX treatment.

Indexed as

DoxorubicinAnimalsApoptosisCardiotoxicityCyclin D2Disease Models, AnimalFibrosisHeart FailureKu AutoantigenMice, Inbred DBAMice, TransgenicMyocytes, CardiacRecovery of FunctionRegenerationSignal TransductionTime FactorsCyclin D2DoxorubicinKu AutoantigenXrcc5 protein, mouseXrcc6 protein, mouseCardiac regenerationCardiomyocyte apoptosisHeart failure

Identifiers

PMID30423020
PMCPMC6452322
OpenAlexW2900551568

What OpenQuestion holds

Textmetadata
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.