Increased Afterload Augments Sunitinib-Induced Cardiotoxicity in an Engineered Cardiac Microtissue Model.
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ABSTRACT:
SUBMITTER: Truitt R
PROVIDER: S-EPMC6059907 | biostudies-literature | 2018 Apr
REPOSITORIES: biostudies-literature
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Increased Afterload Augments Sunitinib-Induced Cardiotoxicity in an Engineered Cardiac Microtissue Model.
Truitt Rachel R Mu Anbin A Corbin Elise A EA Vite Alexia A Brandimarto Jeffrey J Ky Bonnie B Margulies Kenneth B KB
JACC. Basic to translational science 20180401 2
Sunitinib, a multitargeted oral tyrosine kinase inhibitor, used widely to treat solid tumors, results in hypertension in up to 47% and left ventricular dysfunction in up to 19% of treated individuals. The relative contribution of afterload toward inducing cardiac dysfunction with sunitinib treatment remains unknown. We created a preclinical model of sunitinib cardiotoxicity using engineered microtissues that exhibited cardiomyocyte death, decreases in force generation, and spontaneous beating at ...[more]
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