ArticleJACC. CardioOncology2025
Inhibition, But Not Depletion, of Erk Signaling Ameliorates Anthracycline-Induced Cardiotoxicity in Zebrafish.
Article in JACC. CardioOncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Refining the Role of ERK Signaling in Anthracycline-Induced Cardiotoxicity.JACC. CardioOncology · 2026Article
- Tight Regulation of Erk Activity Protects From Anthracycline-Induced Cardiotoxicity.JACC. CardioOncology · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
backgroundAnthracycline-induced cardiotoxicity (AIC) is a unique type of cardiomyopathy that limits the clinical use of anthracyclines in cancer therapy. Although several cardiomyopathy-related pathways have been identified, including extracellular signal-regulated kinase (ERK) signaling, pathway-specific interventions for AIC remain unclear.
objectivesThe aim of this study was to investigate the role of Erk signaling in AIC using zebrafish genetics.
methodsA zebrafish model of AIC was used to screen genes in known cardiomyopathy pathways, including Erk signaling. Heterozygous and homozygous mutants were evaluated for their modifying effects on AIC. In parallel, pharmacologic studies with ERK inhibitors were conducted to assess dose-dependent therapeutic effects of Erk inhibition.
resultsmek1
conclusionsAberrant Erk activation contributes to AIC, and controlled Erk inhibition may offer therapeutic benefit, potentially via antiaging mechanisms. However, optimization is essential, as excessive inhibition can be cardiotoxic.
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