Tanshinone IIA mitigates doxorubicin-induced cardiotoxicity through multifaceted mechanisms including alleviating oxidative stress, inhibiting apoptosis, suppressing inflammation, and modulating autophagy.
Tanshinone IIA and its advanced drug delivery systems represent a promising preclinical strategy for mitigating doxorubicin-induced cardiotoxicity and heart failure.
Doxorubicin (DOX)-induced cardiotoxicity significantly impairs patients' quality of life and long-term prognosis, and can lead to irreversible cardiac dysfunction and heart failure years or even decades after chemotherapy has ceased. Natural medicinal products represent a promising strategy for preventing or treating this cardiotoxicity, with Salvia miltiorrhiza (Danshen) demonstrating therapeutic properties in this context. Considerable attention has been focused on Tanshinone IIA, the principal lipophilic diterpenoid quinone compound found in Danshen, for its potential efficacy against doxorubicin-induced cardiac injury. Its therapeutic mechanisms include alleviating oxidative stress, inhibiting cardiomyocyte apoptosis, exerting anti-inflammatory effects in the myocardium, attenuating cardiac fibrosis, and modulating cardiomyocyte autophagy. This article provides an in-depth elaboration of the mechanisms and targets through which Tan IIA counteracts doxorubicin-induced cardiotoxicity. Furthermore, we explored Tan IIA drug delivery systems (DDS) and device-assisted delivery platforms, thus offering novel insights for future research and clinical translation of Tan IIA, as well as presenting new strategies for addressing doxorubicin-induced cardiac injury.
Wang et al. (Wed,) conducted a review in Doxorubicin-induced cardiotoxicity. Tanshinone IIA was evaluated. Tanshinone IIA mitigates doxorubicin-induced cardiotoxicity through multifaceted mechanisms including alleviating oxidative stress, inhibiting apoptosis, suppressing inflammation, and modulating autophagy.