Evidence map›Paper›PMID 19623174›Full record

ArticleBritish journal of cancer2009

Dexrazoxane-afforded protection against chronic anthracycline cardiotoxicity in vivo: effective rescue of cardiomyocytes from apoptotic cell death.

O Popelová, M Sterba, P Hasková, T Simůnek, M Hroch, I Guncová, P Nachtigal, M Adamcová, V Gersl, Y Mazurová

2 registry-linked trialsOpen access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.3field-weighted citation impact, top 5% 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.

NCT02519335 phase1terminatednot on this mapstarted 2014, after this paper: background citation

Use of the Cardioprotectant Dexrazoxane During Congenital Heart Surgery: Proposal for Pilot Investigation

TypeinterventionalSponsorMedical City Children's HospitalRan2014 to 2017Enrolled12ConditionsHeart Defects, CongenitalArmsDexrazoxane
NCT04997291 phase1unknown statusnot on this mapstarted 2021, after this paper: background citation

Use of the Cardioprotectant Dexrazoxane During Congenital Heart Surgery

TypeinterventionalSponsorUniversity of Texas at AustinRan2021 to 2022Enrolled12ConditionsHeart Defects, CongenitalArmsDexrazoxane
3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 60 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Ferroptosis inhibitors: past, present and future.Frontiers in pharmacology · 2024
    Review
  5. Review
  6. Frontiers in pharmacology · 2023
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
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

10 authors at 1 institution in 1 country.

O PopelováDepartment of Pharmacology, Faculty of Medicine, Charles University in Prague, Simkova 870, Hradec Králové 500 38, Czech Republic.
M Sterba
P Hasková
T Simůnek
M Hroch
I Guncová
P Nachtigal
M Adamcová
V Gersl
Y Mazurová
Charles University · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDexrazoxane (DEX, ICRF-187) is the only clinically approved cardioprotectant against anthracycline cardiotoxicity. It has been traditionally postulated to undergo hydrolysis to iron-chelating agent ADR-925 and to prevent anthracycline-induced oxidative stress, progressive cardiomyocyte degeneration and subsequent non-programmed cell death. However, the additional capability of DEX to protect cardiomyocytes from apoptosis has remained unsubstantiated under clinically relevant in vivo conditions.

methodsChronic anthracycline cardiotoxicity was induced in rabbits by repeated daunorubicin (DAU) administrations (3 mg kg(-1) weekly for 10 weeks). Cardiomyocyte apoptosis was evaluated using TUNEL (terminal deoxynucleotidyl transferase biotin-dUTP nick end labelling) assay and activities of caspases 3/7, 8, 9 and 12. Lipoperoxidation was assayed using HPLC determination of myocardial malondialdehyde and 4-hydroxynonenal immunodetection.

resultsDexrazoxane (60 mg kg(-1)) co-treatment was capable of overcoming DAU-induced mortality, left ventricular dysfunction, profound structural damage of the myocardium and release of cardiac troponin T and I to circulation. Moreover, for the first time, it has been shown that DEX affords significant and nearly complete cardioprotection against anthracycline-induced apoptosis in vivo and effectively suppresses the complex apoptotic signalling triggered by DAU. In individual animals, the severity of apoptotic parameters significantly correlated with cardiac function. However, this effective cardioprotection occurred without a significant decrease in anthracycline-induced lipoperoxidation.

conclusionThis study identifies inhibition of apoptosis as an important target for effective cardioprotection against chronic anthracycline cardiotoxicity and suggests that lipoperoxidation-independent mechanisms are involved in the cardioprotective action of DEX.

Indexed as

AnimalsAnthracyclinesApoptosisCardiotonic AgentsCardiotoxinsHeart DiseasesMaleMyocytes, CardiacRabbitsRazoxaneAnthracyclinesCardiotonic AgentsCardiotoxinsRazoxane

Identifiers

PMID19623174
PMCPMC2736842
OpenAlexW2089186528

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.