Key result
Doxorubicin causes acute cardiomyocyte toxicity and alters genes linked to late-onset cardiotoxicity.
Why the study?
Doxorubicin use is associated with severe cardiotoxicity that can occur years after treatment, and optimal biomarkers for late-onset toxicity are lacking.
Does doxorubicin exposure induce specific biomarker changes in human embryonic stem cell-derived cardiomyocytes?
Population
Human cardiomyocytes derived from embryonic stem cells
Comparison
Doxorubicin exposure at different concentrations vs vehicle control
Design
Preclinical experimental study
Authors
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Does not support clinical biomarker adoption; leaves open predictive value for late doxorubicin cardiotoxicity in patients.
Does doxorubicin exposure induce specific biomarker changes in human embryonic stem cell-derived cardiomyocytes?
Global transcriptional profiling identified novel gene clusters that may serve as sensitive biomarkers for late-onset doxorubicin-induced cardiotoxicity, whereas cTnT is useful for acute toxicity.
Holmgren et al. (2014) studied doxorubicin-induced cardiotoxicity. Doxorubicin vs. vehicle control was evaluated on cytotoxicity (LDH leakage), cTnT release, and global transcriptional profiles. Doxorubicin exposure in human embryonic stem cell-derived cardiomyocytes induced acute cytotoxicity and altered gene expression profiles that may serve as biomarkers for late-onset cardiotoxicity.
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