Do therapeutic modalities targeting Nrf2 prevent or ameliorate doxorubicin-induced cardiotoxicity?
Nrf2 activation is highlighted as a promising therapeutic target to mitigate doxorubicin-induced cardiotoxicity.
Being a broad-spectrum anticancer drug, doxorubicin is indispensable for clinical treatment. Unexpectedly, its cardiotoxic side effects have proven to be a formidable obstacle. Numerous studies are currently devoted to elucidating the pathological mechanisms underlying doxorubicin-induced cardiotoxicity. Nrf2 has always played a crucial role in oxidative stress, but numerous studies have demonstrated that it also plays a vital part in pathological mechanisms like cell death and inflammation. Numerous studies on the pathological mechanisms associated with doxorubicin-induced cardiotoxicity demonstrate this. Several clinical drugs, natural and synthetic compounds, as well as small molecule RNAs have been demonstrated to prevent doxorubicin-induced cardiotoxicity by activating Nrf2. Consequently, this study emphasizes the introduction of Nrf2, discusses the role of Nrf2 in doxorubicin-induced cardiotoxicity, and concludes with a summary of the therapeutic modalities targeting Nrf2 to ameliorate doxorubicin-induced cardiotoxicity, highlighting the potential value of Nrf2 in doxorubicin-induced cardiotoxicity.
Zhao et al. (Wed,) studied this question.