Evidence map›Paper›PMID 26168714›Full record

GuidelineHeart failure reviews2015

Improving the preclinical models for the study of chemotherapy-induced cardiotoxicity: a Position Paper of the Italian Working Group on Drug Cardiotoxicity and Cardioprotection.

Rosalinda Madonna, Christian Cadeddu, Martino Deidda, Donato Mele, Ines Monte, Giuseppina Novo, Pasquale Pagliaro, Alessia Pepe, Paolo Spallarossa, Carlo Gabriele Tocchetti and 2 more

Open access · greenAbstract readGuideline
PubMed Publisher
In one paragraph

Guideline in Heart failure reviews, 2015. 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
5.5field-weighted citation impact, top 3% 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, 45 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
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  8. Article
  9. Mitochondrial Transplantation for Ischemia Reperfusion Injury.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
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  12. Review
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  18. Observational
  19. VEGF-B gene therapy inhibits doxorubicin-induced cardiotoxicity by endothelial protection.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  20. Review
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

12 authors at 10 institutions in 1 country.

Rosalinda MadonnaCenter of Excellence on Aging, Institute of Cardiology, "G. d'Annunzio" University - Chieti, Chieti, Italy, rmadonna@unich.it.
Christian Cadeddu
Martino Deidda
Donato Mele
Ines Monte
Giuseppina Novo
Pasquale Pagliaro
Alessia Pepe
Paolo Spallarossa
Carlo Gabriele Tocchetti
Concetta Zito
Giuseppe Mercuro
University of Cagliari · ITFederico II University Hospital · ITFondazione Toscana Gabriele Monasterio · ITOspedale Policlinico San Martino · ITUniversity of Catania · ITUniversity of Chieti-Pescara · ITUniversity of Ferrara · ITUniversity of Messina · ITUniversity of Palermo · ITUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although treatment for heart failure induced by cancer therapy has improved in recent years, the prevalence of cardiomyopathy due to antineoplastic therapy remains significant worldwide. In addition to traditional mediators of myocardial damage, such as reactive oxygen species, new pathways and target cells should be considered responsible for the impairment of cardiac function during anticancer treatment. Accordingly, there is a need to develop novel therapeutic strategies to protect the heart from pharmacologic injury, and improve clinical outcomes in cancer patients. The development of novel protective therapies requires testing putative therapeutic strategies in appropriate animal models of chemotherapy-induced cardiomyopathy. This Position Paper of the Working Group on Drug Cardiotoxicity and Cardioprotection of the Italian Society of Cardiology aims to: (1) define the distinctive etiopatogenetic features of cardiac toxicity induced by cancer therapy in humans, which include new aspects of mitochondrial function and oxidative stress, neuregulin-1 modulation through the ErbB receptor family, angiogenesis inhibition, and cardiac stem cell depletion and/or dysfunction; (2) review the new, more promising therapeutic strategies for cardioprotection, aimed to increase the survival of patients with severe antineoplastic-induced cardiotoxicity; (3) recommend the distinctive pathological features of cardiotoxicity induced by cancer therapy in humans that should be present in animal models used to identify or to test new cardioprotective therapies.

Indexed as

CardiotoxicityAnimalsAntineoplastic AgentsCardiotonic AgentsDisease Models, AnimalHumansMitochondria, HeartNeoplasmsNeuregulin-1Oxidative StressAntineoplastic AgentsCardiotonic AgentsNeuregulin-1NRG1 protein, human

Identifiers

PMID26168714
OpenAlexW2173100112

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.