Key result
Urolithin A mitigates doxorubicin-induced myocardial injury in preclinical models by inhibiting ROS-driven apoptosis.
Why the study?
Does Urolithin A mitigate doxorubicin-induced myocardial injury in preclinical models?
Does Urolithin A mitigate doxorubicin-induced myocardial injury in preclinical models?
Answers are grounded in this paper and cite their sources.
Urolithin A demonstrates preclinical potential to protect against doxorubicin-induced cardiotoxicity by suppressing ROS-driven apoptosis.
Our findings validated the rational design that UA has the potential to mitigate DOX-induced myocardial injury in vitro and in vivo by inhibiting ROS-driven apoptosis, which yields significant insights for combating DOX-mediated myocardial injury.
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Song et al. (2026) studied this question. Urolithin A mitigated doxorubicin-induced myocardial injury by inhibiting ROS-driven apoptosis both in vitro and in vivo.
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