Evidence map›Paper›PMID 35333943›Full record

ReviewArchives of toxicology2022

Molecular insights into the pathophysiology of doxorubicin-induced cardiotoxicity: a graphical representation.

Nonhlakanipho F Sangweni, Kwazi Gabuza, Barbara Huisamen, Lawrence Mabasa, Derick van Vuuren, Rabia Johnson

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Archives of toxicology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
13.5field-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

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

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. EV-Encapsulated Mitochondrial miRNAs: Enhancing Cardiomyocyte Bioenergetics.International journal of molecular sciences · 2026
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. CIRBP StabilizesAntioxidants (Basel, Switzerland) · 2025
    Article
  14. Mitochondrial Amount Determines Doxorubicin-Induced Cardiotoxicity in Cardiomyocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  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

6 authors at 2 institutions in 1 country.

Nonhlakanipho F SangweniBiomedical Research and Innovation Platform, South African Medical Research Council, Tygerberg, P.O. Box 19070, Cape Town, 7505, South Africa.ORCID http://orcid.org/0000-0002-8400-3967
Kwazi GabuzaBiomedical Research and Innovation Platform, South African Medical Research Council, Tygerberg, P.O. Box 19070, Cape Town, 7505, South Africa.
Barbara HuisamenCentre for Cardio-Metabolic Research in Africa, Division of Medical Physiology, Faculty of Medicine and Health Sciences, Stellenbosch University, Tygerberg, 7505, South Africa.
Lawrence MabasaBiomedical Research and Innovation Platform, South African Medical Research Council, Tygerberg, P.O. Box 19070, Cape Town, 7505, South Africa.
Derick van VuurenCentre for Cardio-Metabolic Research in Africa, Division of Medical Physiology, Faculty of Medicine and Health Sciences, Stellenbosch University, Tygerberg, 7505, South Africa.
Rabia JohnsonBiomedical Research and Innovation Platform, South African Medical Research Council, Tygerberg, P.O. Box 19070, Cape Town, 7505, South Africa. rabia.johnson@mrc.ac.za.
South African Medical Research Council · ZAStellenbosch University · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A breakthrough in oncology research was the discovery of doxorubicin (Dox) in the 1960's. Unlike other chemotherapy drugs, Dox was determined to have a greater therapeutic index. Since its discovery, Dox has, in part, contributed to the 5-10-year survival increase in cancer patient outcomes. Unfortunately, despite its efficacy, both in adult and pediatric cancers, the clinical significance of Dox is tainted by its adverse side effects, which usually manifest as cardiotoxicity. The issue stems from Dox's lack of specificity which prevents it from accurately distinguishing between cancer cells and healthy cell lines, like cardiomyocytes. In addition, the high binding affinity of Dox to topoisomerases, which are abundantly found in cancer and cardiac cells in different isoforms, potentiates DNA damage. In both cell lines, Dox induces cytotoxicity by stimulating the production of pro-oxidants whilst inhibiting antioxidant enzymatic activity. Given that the cardiac muscle has an inherently low antioxidant capacity makes it susceptible to oxidative damage thereby, allowing the accumulation of Dox within the myocardium. Subsequently, Dox drives the activation of cell death pathways, such as ferroptosis, necroptosis and apoptosis by triggering numerous cellular responses that have been implicated in diseases. To date, the exact mechanism by which Dox induces the cardiotoxicity remains an aspect of much interest in cardio-oncology research. Hence, the current review summarizes the proposed mechanisms that are associated with the onset and progression of DIC.

Indexed as

AntioxidantsCardiotoxicityApoptosisChildDoxorubicinHumansMyocytes, CardiacOxidative StressAntioxidantsDoxorubicinCell death pathwaysDoxorubicin-induced cardiotoxicityEndogenous antioxidants

Identifiers

PMID35333943
PMCPMC9095530
OpenAlexW4220805090

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.