Increased Afterload Augments Sunitinib-Induced Cardiotoxicity in an Engineered Cardiac Microtissue Model.
JACC Basic Transl Sci
; 3(2): 265-276, 2018 Apr.
Article
en En
| MEDLINE
| ID: mdl-30062212
2D, 2-dimensional; 3D, 3-dimensional; AICAR, 5-aminoimidazole-4-carboxamide 1-ß-D-ribofuranoside; AMPK, adenosine monophosphate-activated protein kinase; ATP, adenosine triphosphate; CCCP, carbonyl cyanide m-chlorophenyl hydrazine; CMT, cardiac microtissue; DMSO, dimethyl sulfoxide; EDTA, ethylenediamine tetraacetic acid; Hu-iPS-CM, human induced pluripotent stem cell cardiomyocyte; LV, left ventricle; NRVM, neonatal rat ventricular myocyte; PDMS, polydimethylsiloxane; RPMI, Roswell Park Memorial Institute medium; TMRM, tetramethylrhodamine; afterload; apoptosis; cardiotoxicity; huMSC, human mesenchymal stem cell; iPS-CM, induced pluripotent stem cell-derived cardiomyocyte; sunitinib; tissue engineering; toxicology; tyrosine kinase inhibitors
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01-internacional
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MEDLINE
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En
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JACC Basic Transl Sci
Año:
2018
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Article