Key result
Specific ablation of Slc25a49 exacerbated Doxorubicin-induced cardiomyopathy via the G6P–AP-1–Sln axis, while targeting this axis with the AP-1 inhibitor T-5224 improved survival and cardiac function.
Why the study?
Few mechanism-based therapies exist for doxorubicin cardiotoxicity, prompting investigation into specific mechanisms of mitochondrial energy reprogramming in doxorubicin-induced cardiomyopathy.
Does targeting the G6P-AP-1-Sln axis with T-5224 improve survival and cardiac function in doxorubicin-induced cardiomyopathy models?
Population
Cardiac-specific Slc25a49 knockout mice and SLC25A49 knockdown cardiomyocytes
Comparison
Doxorubicin treatment and AP-1 inhibitor T-5224
Design
Preclinical mechanistic animal and in vitro study
Authors
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Opens a potential therapeutic avenue for doxorubicin cardiotoxicity; leaves open clinical translation of T-5224.
Does targeting the G6P-AP-1-Sln axis with T-5224 improve survival and cardiac function in doxorubicin-induced cardiomyopathy models?
Targeting the G6P-AP-1-Sln axis with the AP-1 inhibitor T-5224 improves survival and cardiac function in a preclinical model of doxorubicin-induced cardiomyopathy.
Wan et al. (2025) studied Doxorubicin-induced cardiomyopathy. Cardiac-specific ablation of Slc25a49 and AP-1 inhibitor T-5224 was evaluated on Myocardial damage, survival, and cardiac function. Specific ablation of Slc25a49 exacerbated Doxorubicin-induced cardiomyopathy via the G6P–AP-1–Sln axis, while targeting this axis with the AP-1 inhibitor T-5224 improved survival and cardiac function.
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