Evaluation of Senescence and Its Prevention in Doxorubicin-Induced Cardiotoxicity Using Dynamic Engineered Heart Tissues

Annet N. Linders, Itamar B. Dias, Ekaterina S. Ovchinnikova, Mathilde C.S.C. Vermeer, Martijn F. Hoes, George Markousis Mavrogenis, Frederik E. Deiman, Karla F. Arevalo Gomez, Jacqueline M. Bliley, Jamil Nehme, Aryan Vink, Jourik Gietema, Rudolf A. de Boer, Daan Westenbrink, Herman H.W. Sillje, Denise Hilfiker-Kleiner, Linda W. van Laake, Adam W. Feinberg, Marco Demaria, Nils BomerPeter van der Meer*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

10 Citations (Scopus)
110 Downloads (Pure)

Abstract

Background: Doxorubicin is an essential cancer treatment, but its usefulness is hampered by the occurrence of cardiotoxicity. Nevertheless, the pathophysiology underlying doxorubicin-induced cardiotoxicity and the respective molecular mechanisms are poorly understood. Recent studies have suggested involvement of cellular senescence.

Objectives: The aims of this study were to establish whether senescence is present in patients with doxorubicin-induced cardiotoxicity and to investigate if this could be used as a potential treatment target.

Methods: Biopsies from the left ventricles of patients with severe doxorubicin-induced cardiotoxicity were compared with control samples. Additionally, senescence-associated mechanisms were characterized in 3-dimensional dynamic engineered heart tissues (dyn-EHTs) and human pluripotent stem cell–derived cardiomyocytes. These were exposed to multiple, clinically relevant doses of doxorubicin to recapitulate patient treatment regimens. To prevent senescence, dyn-EHTs were cotreated with the senomorphic drugs 5-aminoimidazole-4-carboxamide ribonucleotide and resveratrol.

Results: Senescence-related markers were significantly up-regulated in the left ventricles of patients with doxorubicin-induced cardiotoxicity. Treatment of dyn-EHTs resulted in up-regulation of similar senescence markers as seen in the patients, accompanied by tissue dilatation, decreased force generation, and increased troponin release. Treatment with senomorphic drugs led to decreased expression of senescence-associated markers, but this was not accompanied by improved function.

Conclusions: Senescence was observed in the hearts of patients with severe doxorubicin-induced cardiotoxicity, and this phenotype can be modeled in vitro by exposing dyn-EHTs to repeated clinically relevant doses of doxorubicin. The senomorphic drugs 5-aminoimidazole-4-carboxamide ribonucleotide and resveratrol prevent senescence but do not result in functional improvements. These findings suggest that preventing senescence by using a senomorphic during doxorubicin administration might not prevent cardiotoxicity.

Original languageEnglish
Pages (from-to)298-315
Number of pages18
JournalJacc: cardiooncology
Volume5
Issue number3
DOIs
Publication statusPublished - Jun-2023

Keywords

  • cardiotoxicity
  • doxorubicin
  • hPSC-derived cardiomyocytes
  • senescence
  • senomorphic drugs

Fingerprint

Dive into the research topics of 'Evaluation of Senescence and Its Prevention in Doxorubicin-Induced Cardiotoxicity Using Dynamic Engineered Heart Tissues'. Together they form a unique fingerprint.

Cite this