Key result
Doxorubicin administration (3 mg/kg/d for 5 days) induced cardiac dysfunction and injury in mice, linked to increased inflammatory cytokines and distinct transcriptomic and metabolomic changes.
Why the study?
Doxorubicin clinical utility is limited by dose-dependent cardiotoxicity, and while inflammatory responses have been implicated, the exact mechanism remains unknown.
Population
Male C57BL/6 J mice (8 weeks old)
Comparison
Continuous intraperitoneal DOX injections (3 mg/kg/d) for five days vs controls
Design
Animal study
Follow-up
five days
Authors
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Hypothesis-generating for IL-17/TNF-targeted cardioprotection in doxorubicin toxicity; leaves open human translation and trials.
Multi-omics analysis reveals that doxorubicin-induced cardiotoxicity in mice is strongly associated with inflammatory responses, specifically IL-17 and TNF signaling pathways, and specific lipid/metabolite alterations.
Tan et al. (2023) studied Doxorubicin-induced cardiotoxicity. Doxorubicin was evaluated on Cardiac dysfunction, cardiac injury, and multi-omics changes. Doxorubicin administration (3 mg/kg/d for 5 days) induced cardiac dysfunction and injury in mice, linked to increased inflammatory cytokines and distinct transcriptomic and metabolomic changes.
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