Abstract #4696

Probing Mitochondrial Dysfunction in Mouse Hearts with Doxorubicin-Induced Cardiotoxicity Using Ungated 4D Oxy-wavelet MRI

Devin Raine Everaldo Cortes^1,2,3, Margaret C. Stapleton^2,3, Kristina E. Schwab^4,5, Noah W. Coulson^2,3, Elizabeth Mazzella^2,3,6, Dalton R West^2,3, Thomas Becker-Szurszewski^3,7, Sean Hartwick^3,4, Anthony G. Christodoulou⁸, and Yijen L Wu^1,2,3,7

¹Department of Bioengineering, Swanson School of Engineering, University of Pittsburgh, Pittsburgh, PA, United States, ²Department of Developmental Biology, School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States, ³Rangos Research Center Small Animal Imaging Core, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA, United States, ⁴Rangos Research Center Animal Imaging Core, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA, United States, ⁵Department of Pediatrics, University of Pittsburgh, School of Medicine, Pittsburgh, PA, United States, ⁶Department of Chemistry, Dietrich School of Arts and Sciences, University of Pittsburgh, Pittsburgh, PA, United States, ⁷Department of Pediatrics, School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States, ⁸Biomedical Imaging Research Institue, Cedars-Sinai Medical Center, Los Angeles, CA, United States

Synopsis

Keywords: Heart, Toxicity, 4D fMRI, Doxorubicin, cardiomyopathyCardiomyopathy caused by anti-cancer anthracyclines, such as Doxorubicin (Dox), is one major cause for long-term morbidity and mortality among cancer survivors. Patients can develop cardiomyopathy leading to heart failure decades after successful cancer treatment with Dox. There is an urgent need for early detection of sub-clinical pathogenesis of Dox-induced cardiotoxicity for early intervention before irreversible cardiac tissue damage occurs. Cellular mechanistic investigations showed that mitochondrial dysfunctions are central to the Dox-induced cardiotoxicity. We have developed a time-and-motion-resolved 4D Oxy-wavelet MRI capable of detecting early Dox-induced mitochondrial dysfunction in the heart before irreversible myocardial damage occurred.

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