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In summary, DOX is a very valuable cancer chemotherapeutic drug that frequently results in severe cardiomyopathy. The ability of SFN to protect against DOX cardiotoxicity, as shown for the first time by the results of our study, is a discovery that could significantly change the way DOX is currently used. Our findings not only provide further insight into DOX-induced cardiotoxicity, but especially demonstrate SFN action through the Keap1/Nrf2 signaling pathway for countering cardiac damage. Our observations should establish the basis for devising novel approaches to protect the human heart from the harmful effects of cardiotoxic drugs, which are thought to be mediated in part by oxidative stress signaling.

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