Key result
Trastuzumab abrogates hCDC functional benefits in infarcted mouse hearts, worsening ejection fraction and scar thickness.
Why the study?
Trastuzumab cardiotoxicity may involve inhibition of human adult cardiac-derived stem cells in addition to direct adverse effects on cardiomyocytes.
Does Trastuzumab impair the regenerative function of human resident cardiac stem cells?
Population
Human cardiosphere-derived cells in vitro and acutely infarcted mouse hearts (n=12 per group)
Comparison
Trastuzumab-treated cells or mice vs untreated cells or hCDCs alone
Design
Preclinical in vitro and in vivo study
Authors
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TZM may impair cardiac stem cell function; leaves open contribution to clinical cardiotoxicity.
Does Trastuzumab impair the regenerative function of human resident cardiac stem cells?
Trastuzumab impairs the cardiomyogenic and angiogenic capacities of human resident cardiac stem cells, providing a potential novel mechanism for its cardiotoxicity.
Barth et al. (2012) studied Cardiotoxicity (n=24). Trastuzumab vs. hCDCs alone was evaluated on Ejection fraction, infarct scar thickness, and capillary density. Trastuzumab abrogated the functional benefits of human cardiosphere-derived cells in acutely infarcted mouse hearts (n=12 per group), resulting in lower ejection fraction and thinner infarct scar.
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