Evidence map›Paper›PMID 27213178›Full record

ArticleInternational journal of cardiology. Heart & vasculature2016

Doxorubicin induced heart failure: Phenotype and molecular mechanisms.

Maria A Mitry, John G Edwards

Open access · goldAbstract read
In one paragraph

Article in International journal of cardiology. Heart & vasculature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers.

0numbers the graph read from it
0cells of the map it votes in
155citing papers in PubMed
10.6field-weighted citation impact, top 1% 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

155 citing papers in PubMed, 315 citations in OpenAlex.

  1. Article
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  3. Chemo-/radiotherapy-induced cardiomyopathy: roles of mitochondria and endoplasmic reticulum.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2026
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  16. 2-[Molecular imaging and biology · 2025
    Article
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95 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

2 authors at 1 institution in 1 country.

Maria A MitryDepartment of Physiology, New York Medical College, Valhalla, NY, United States.
John G EdwardsDepartment of Physiology, New York Medical College, Valhalla, NY, United States.
New York Medical College · US

Funding

Doxorubicin-induced cardiac progenitor cell death is antecedent to heart failure.R03HD065551 · NICHD · NEW YORK MEDICAL COLLEGE · PI EDWARDS, JOHN G · 2010 to 2010
$80k
NICHD NIH HHS R03 HD065551
6 · The paper itself

Abstract

Long term survival of childhood cancers is now more than 70%. Anthracyclines, including doxorubicin, are some of the most efficacious anticancer drugs available. However, its use as a chemotherapeutic agent is severely hindered by its dose-limiting toxicities. Most notably observed is cardiotoxicity, but other organ systems are also degraded by doxorubicin use. Despite the years of its use and the amount of information written about this drug, an understanding of its cellular mechanisms is not fully appreciated. The mechanisms by which doxorubicin induces cytotoxicity in target cancer cells have given insight about how the drug damages cardiomyocytes. The major mechanisms of doxorubicin actions are thought to be as an oxidant generator and as an inhibitor of topoisomerase 2. However, other signaling pathways are also invoked with significant consequences for the cardiomyocyte. Further the interaction between oxidant generation and topoisomerase function has only recently been appreciated and the consequences of this interaction are still not fully understood. The unfortunate consequences of doxorubicin within cardiomyocytes have promoted the search for new drugs and methods that can prevent or reverse the damage caused to the heart after treatment in cancer patients. Alternative protocols have lessened the impact on newly diagnosed cancer patients. However the years of doxorubicin use have generated a need for monitoring the onset of cardiotoxicity as well as understanding its potential long-term consequences. Although a fairly clear understanding of the short-term pathologic mechanisms of doxorubicin actions has been achieved, the long-term mechanisms of doxorubicin induced heart failure remain to be carefully delineated.

Indexed as

CancerCardiomyopathyDNA damageDoxorubicinHeart failureMitochondriaOxidant stressTopoisomerase

Identifiers

PMID27213178
PMCPMC4871279
OpenAlexW2173735004

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.