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With earlier-stage cancer diagnosis and improved efficacy of chemotherapy, doxorubicin-induced cardiotoxicity has increasingly become a significa nt cause of morbidity and mortality among cancer survivors. For example, the cardiac mortality of long-term pediatric cancer survivors is estimated to be more than eight times higher than expected. A major challenge in reducing therapy-associated cardiotoxicity is the paucity of knowledge about the molecular players and pathways that can mitigate the undesired effects of doxorubicin on myocardium.

UT Health San Antonio
Li, Rong