Quizartinib promotes cardiac inflammation that contributes to cardiotoxicity

Clicks: 1
ID: 323279
2026
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal

Ranked #93 of 282 articles by views in European heart journal supplements : journal of the European Society of Cardiology

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 282 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Abstract Introduction Cardiotoxicity has emerged as a major complication of modern cancer therapies including tyrosine kinase inhibitors (TKIs). Quizartinib, a FLT3 targeting TKI, leads to adverse cardiovascular events in patients; however, the mechanisms underlying this cardiotoxicity remain elusive. Methods We combined in vitro and in vivo approaches to investigate the effects of quizartinib on cardiomyocyte homeostasis and cardiac function. In vitro, cultured cardiomyocytes were treated with quizartinib to assess cell viability, metabolic function, and the expression of stress- and inflammation-related genes. In vivo, a murine myocardial infarction (MI) model was used to represent a disease-sensitized myocardium reflective of cancer patients with underlying cardiovascular comorbidities. Mice treated with quizartinib, or vehicle were subjected to MI and cardiac function was assessed by echocardiography and fibrosis up to four weeks post-MI. Bulk RNA sequencing was performed on cardiac tissue collected one-week post-MI and cardiac immune cell populations were quantified by flow cytometry for immune profiling. Results Quizartinib treatment reduced cardiomyocyte viability and altered the expression of genes associated with cellular stress, mitochondrial function, and inflammatory signalling. In healthy mice, quizartinib increased cardiac infiltration of innate immune cells, particularly neutrophils and monocytes. Moreover, in the MI model, quizartinib further exacerbated cardiac dysfunction as previously shown as well as cardiac inflammation. Transcriptomic analysis revealed enrichment of interferon signalling and leukocyte migration pathways, alongside down regulation of oxidative phosphorylation, ATP production, and cardiac muscle contraction pathways in quizartinib-treated compared to vehicle-treated infarcted hearts, consistent with more pronounced impairment of metabolic and contractile function. Conclusions These findings demonstrate that quizartinib induces cardiomyocyte stress and promotes cardiac inflammation, which together contribute to impaired cardiac repair and more severe dysfunction after injury. This study identifies inflammation as a key mechanistic component of quizartinib-associated cardiotoxicity and provides a rationale for targeting inflammatory pathways to mitigate cardiovascular risk during therapy.
Reference Key
openalex_W7172298513 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Y Alshoubaki, R Bernasconi, A Gustinelli, V Gruterich, L Xu, V Lorenz, J Roux, L Wigger, S Calderon, T Pedrazzini, G M Kuster
Journal European heart journal supplements : journal of the European Society of Cardiology
Year 2026
DOI
10.1093/eurheartjsupp/suag097.216
URL
https://doi.org/10.1093/eurheartjsupp/suag097.216
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.