The CMPK2–mtDNA axis mediates doxorubicin cardiotoxicity: mechanistic links to STAT1 transcription and FAD-mediated inhibition
Doxorubicin is a widely used chemotherapeutic agent whose clinical utility is limited by dose-dependent cardiotoxicity. The precise mechanisms bridging mitochondrial dysfunction to cardiac inflammatory responses remain poorly defined. We utilized cardiomyocyte-specific CMPK2 knockout and overexpression mou...