The solute carrier superfamily comprises of uptake transporters that can contribute to the absorption and elimination of a broad array of clinically important drugs. Recent studies have suggested that the tissue-specific expression of these transporters may have important consequences for an individual's susceptibility to drug-induced organ damage or to drug-drug interactions. Polymorphic variants have been identified in genes encoded by this family, and some of these have been associated with functional changes in transport function and response to anthracycline-induced toxicity and efficacy. Here, we review recent advances in the role solute carrier transporters play in anthracycline-induced cardiotoxicity, highlight potential implications of genetic variants that may contribute to drug response and discuss novel technologies to study mechanisms of anthracycline transport.
Keywords: anthracyclines; cardiomyocytes; cardiotoxicity; doxorubicin; organic cation transporters; solute carriers.