Key result
HSF-1 knockout reduces doxorubicin-induced heart failure and improves survival in mice.
Why the study?
Does HSF-1 knockout prevent doxorubicin-induced heart failure in mice?
Population
HSF-1 wild-type (HSF-1(+/+)) and knock-out (HSF-1(-/-)) mice
Comparison
Doxorubicin (Dox) treatment vs HSF-1(+/+) vs HSF-1(-/-) mice
Design
Preclinical
Authors
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HSF-1 knockout attenuates doxorubicin cardiotoxicity in mice; hypothesis-generating for inhibition as a strategy in anthracycline-treated patients.
Does HSF-1 knockout prevent doxorubicin-induced heart failure in mice?
HSF-1 activation mediates doxorubicin-induced heart failure via Hsp25-induced p53 transactivation and increased Bax levels, suggesting a novel mechanism for anthracycline cardiotoxicity.
Vedam et al. (2010) studied Doxorubicin-induced heart failure. HSF-1 knockout (HSF-1(-/-)) vs. HSF-1 wild-type (HSF-1(+/+)) was evaluated on Doxorubicin-induced heart failure and survival rate. HSF-1(-/-) mice showed significantly reduced doxorubicin-induced heart failure and a higher survival rate compared to wild-type mice.
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