Transient cardiomyopathy by tyrosine kinase inhibitor therapy: time to define a new syndrome in cardio-oncology?

This editorial refers to ‘Osimertinib induces reversible cardiac dysfunction through the GATA4-MYLK3-MYL2 axis’, by K. Zhang et al., https://doi.org/10.1093/eurheartj/ehaf813.For years, cardiotoxicity has been viewed largely through the lens of irreversible dysfunction. However, emerging evidence no...

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Bibliographic Details
Main Author: Lehmann, Lorenz (Author)
Format: Article (Journal) Editorial
Language:English
Published: 03 December 2025
In: European heart journal
Year: 2025, Pages: 1-3
ISSN:1522-9645
DOI:10.1093/eurheartj/ehaf869
Online Access:Verlag, kostenfrei, Volltext: https://doi.org/10.1093/eurheartj/ehaf869
Verlag, kostenfrei, Volltext: https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehaf869/8363059?login=true
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Author Notes:Lorenz H Lehmann
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Summary:This editorial refers to ‘Osimertinib induces reversible cardiac dysfunction through the GATA4-MYLK3-MYL2 axis’, by K. Zhang et al., https://doi.org/10.1093/eurheartj/ehaf813.For years, cardiotoxicity has been viewed largely through the lens of irreversible dysfunction. However, emerging evidence now paints a more nuanced picture: not all myocardial injury is permanent. The first data for reversibility of drug-induced cardiac dysfunction came from targeted therapies against surface receptors that signal proliferation pathways via their intracellular tyrosine kinase activity, such as the epidermal growth factor receptor (EGFR).1 While these receptors can be inhibited in their extracellular domain via antibodies, the plethora of drugs has shifted to direct tyrosine kinase inhibitors (TKIs).2 These small molecules, in addition to their desired target, often hit multiple ‘off-targets’.3 For obvious reasons, these intricacies have obscured molecular mechanistic insight into the toxicities of TKIs such as those pertaining to the cardiovascular system.
Item Description:Gesehen am 25.02.2026
Physical Description:Online Resource
ISSN:1522-9645
DOI:10.1093/eurheartj/ehaf869