Evidence map›Paper›PMID 33547494›Full record

ReviewCurrent treatment options in oncology2021

Metabolic Aspects of Anthracycline Cardiotoxicity.

Michele Russo, Angela Della Sala, Carlo Gabriele Tocchetti, Paolo Ettore Porporato, Alessandra Ghigo

Open access · hybridAbstract readReview
In one paragraph

Review in Current treatment options in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
11.0field-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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
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  7. Article
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  11. Article
  12. Article
  13. Triaptosis and Cancer: Next Hope?Research (Washington, D.C.) · 2025
    Review
  14. Doxorubicin-induced cardiometabolic disturbances: what can we do?Frontiers in clinical diabetes and healthcare · 2025
    Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

1 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

5 authors at 2 institutions in 1 country.

Michele Russo *Department of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center, University of Torino, Torino, Via Nizza 52, 10126, Torino, Italy.
Angela Della Sala *Department of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center, University of Torino, Torino, Via Nizza 52, 10126, Torino, Italy.
Carlo Gabriele TocchettiDepartment of Translational Medical Sciences, Federico II University, Naples, Italy.
Paolo Ettore PorporatoDepartment of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center, University of Torino, Torino, Via Nizza 52, 10126, Torino, Italy.
Alessandra GhigoDepartment of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center, University of Torino, Torino, Via Nizza 52, 10126, Torino, Italy. Alessandra.ghigo@unito.it.ORCID 0000-0002-1193-5296
University of Turin · ITFederico II University Hospital · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

opinion statementHeart failure (HF) is increasingly recognized as the major complication of chemotherapy regimens. Despite the development of modern targeted therapies such as monoclonal antibodies, doxorubicin (DOXO), one of the most cardiotoxic anticancer agents, still remains the treatment of choice for several solid and hematological tumors. The insurgence of cardiotoxicity represents the major limitation to the clinical use of this potent anticancer drug. At the molecular level, cardiac side effects of DOXO have been associated to mitochondrial dysfunction, DNA damage, impairment of iron metabolism, apoptosis, and autophagy dysregulation. On these bases, the antioxidant and iron chelator molecule, dexrazoxane, currently represents the unique FDA-approved cardioprotectant for patients treated with anthracyclines.A less explored area of research concerns the impact of DOXO on cardiac metabolism. Recent metabolomic studies highlight the possibility that cardiac metabolic alterations may critically contribute to the development of DOXO cardiotoxicity. Among these, the impairment of oxidative phosphorylation and the persistent activation of glycolysis, which are commonly observed in response to DOXO treatment, may undermine the ability of cardiomyocytes to meet the energy demand, eventually leading to energetic failure. Moreover, increasing evidence links DOXO cardiotoxicity to imbalanced insulin signaling and to cardiac insulin resistance. Although anti-diabetic drugs, such as empagliflozin and metformin, have shown interesting cardioprotective effects in vitro and in vivo in different models of heart failure, their mechanism of action is unclear, and their use for the treatment of DOXO cardiotoxicity is still unexplored.This review article aims at summarizing current evidence of the metabolic derangements induced by DOXO and at providing speculations on how key players of cardiac metabolism could be pharmacologically targeted to prevent or cure DOXO cardiomyopathy.

Indexed as

AnthracyclinesAntineoplastic AgentsAutophagyBiomarkersCardiotoxicityCell SurvivalDisease SusceptibilityFatty AcidsGlycolysisHumansInsulin ResistanceIronMyocardiumMyocytes, CardiacNeoplasmsOxidation-ReductionAnthracyclinesAntineoplastic AgentsBiomarkersFatty AcidsIronCardiac metabolismCardiotoxicityDoxorubicin

Identifiers

PMID33547494
PMCPMC7864817
OpenAlexW3126300637

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.