Abstract
The chemotherapeutic doxorubicin is the most frequently prescribed anticancer drug and is given as a single agent or in combination with other antitumor drugs. Administration of doxorubicin can lead to both short- and long-term cardiotoxic effects, ranging from subclinical alterations of myocardial structure and function to severe cardiomyopathy and heart failure, which may result in heart transplantation or death. In this issue of Molecular Therapy, Chatterjee et al.1 address this key challenge in cardio-oncology by demonstrating that adeno-associated virus 9 (AAV9)-mediated gene transfer of murine telomerase reverse transcriptase (Tert) under control of the cardiomyocyte-specific cardiac troponin T promoter (AAV9-Tert) prevents cardiac atrophy and systolic dysfunction in a murine model of chronic doxorubicin cardiotoxicity.
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