Evidence map›Paper›PMID 31488712›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

p53 prevents doxorubicin cardiotoxicity independently of its prototypical tumor suppressor activities.

Jie Li, Ping-Yuan Wang, Nathaniel A Long, Jie Zhuang, Danielle A Springer, Jizhong Zou, Yongshun Lin, Christopher K E Bleck, Ji-Hoon Park, Ju-Gyeong Kang and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
7.7field-weighted citation impact, top 2% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

  1. Pooled it
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  17. PARP-2 mediates cardiomyocyte aging and damage induced by doxorubicin through SIRT1 Inhibition.Apoptosis : an international journal on programmed cell death · 2024
    Article
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  19. NAD in pathological cardiac remodeling: Metabolic regulation and beyond.Biochimica et biophysica acta. Molecular basis of disease · 2024
    Review
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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 2 institutions in 1 country.

Jie LiCardiovascular Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Ping-Yuan WangCardiovascular Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Nathaniel A LongCardiovascular Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Jie ZhuangCardiovascular Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Danielle A SpringerMurine Phenotyping Core, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Jizhong ZouInduced Pluripotent Stem Cell Core, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Yongshun LinInduced Pluripotent Stem Cell Core, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Christopher K E BleckElectron Microscopy Core, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Ji-Hoon ParkCardiovascular Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Ju-Gyeong KangCardiovascular Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Paul M HwangCardiovascular Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892; hwangp@mail.nih.gov.
National Heart Lung and Blood Institute · USNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Doxorubicin is a widely used chemotherapeutic agent that causes dose-dependent cardiotoxicity in a subset of treated patients, but the genetic determinants of this susceptibility are poorly understood. Here, we report that a noncanonical tumor suppressor activity of p53 prevents cardiac dysfunction in a mouse model induced by doxorubicin administered in divided low doses as in the clinics. While relatively preserved in wild-type (

Indexed as

AnimalsApoptosisCardiomyopathiesCardiotoxicityDNA-Binding ProteinsDNA, MitochondrialDoxorubicinHeart DiseasesHumansInduced Pluripotent Stem CellsMaleMiceMice, Inbred C57BLMice, KnockoutMitochondria, HeartMitochondrial ProteinsDNA-Binding ProteinsDNA, MitochondrialDoxorubicinMitochondrial Proteinsmitochondrial transcription factor ATP53 protein, humanTranscription FactorsTrp53 protein, mouseTumor Suppressor Protein p53anthracyclinecardiomyopathymitochondriamtDNAp53

Identifiers

PMID31488712
PMCPMC6765288
OpenAlexW2971567921

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.