Anthracyclines are cornerstone agents in oncology, yet their cardiotoxic effects may do more than inflict damage-they may uncover latent cardiac vulnerabilities. This mini-review examines anthracycline-induced mitochondrial stress as a potential diagnostic stressor that exposes subclinical impairments in cardiomyocyte energetics and quality control. We focus on receptor-mediated mitophagy, particularly the TRDMT1-BNIP3 epitranscriptomic axis, which enables organelle clearance independently of membrane depolarization, and the canonical PINK1-Parkin pathway, highlighting their distinct and sometimes context-dependent roles. Unlike the canonical PINK1-Parkin pathway, which is typically activated by mitochondrial depolarization, the TRDMT1-BNIP3 axis may better reflect early adaptive responses to specific cellular stresses. We summarize emerging evidence from iPSC-derived cardiomyocytes, animal models, and molecular imaging studies, suggesting that mitochondrial dysfunction precedes overt systolic decline. We propose that doxorubicin-induced effects on mitophagy pathways may serve as a functional indicator of mitochondrial reserve, providing a basis for risk stratification and targeted cardioprotection. Reframing cardiotoxicity as a measurable biological signal-not only as injury-could improve early detection of heart failure susceptibility by revealing these hidden vulnerabilities. These insights are hypothesis-generating and require further clinical validation before implementation in diagnostic frameworks.