Authors: Lindsey R Farris, Rama D Yammani, Leslie B Poole
Published: 2022-11-14
DOI: 10.1161/res.131.suppl_1.p3118
Source: Full article
Chemotherapeutic-induced cardiomyopathies have surpassed cancer as the leading cause of death in patients post-remission. The highly efficacious anti-neoplastic agent, Doxorubicin (DOX), is a major culprit of dose-limiting cardiotoxicity, though the method of insult is not completely understood. While cardiotoxicity is likely multifaceted, a route of interest is the upregulation of reactive oxygen species (ROS) that leads to mitochondrial damage and other cellular complications within cardiomyocytes. Cardiomyocytes are heavily reliant on their mitochondria as the source of cellular energy, as 30% of cell volume is taken up by the organelle. To understand and counter ROS accumulation in the mitochondria with DOX administration, we are investigating the role of mitochondrially targeted antioxidants. We have found that DOX increases cytotoxicity and caspase-3 cleavage in cardiomyoblasts