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In a rat model of DOX-induced cardiotoxicity, it has been unequivocally demonstrated that DOX induces the production of ROS and transforming growth factor-beta (TGF-), thereby promoting the transformation of cardiac fibroblasts into myofibroblasts (Tian et al., 2024)

This leads to disruptions in the transcription of proteins vital to the mitochondrial ETC, thus inducing malfunction and hindering ATP synthesis, which in turn might escalate ROS generation [113]

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5.2.2 F2 generation effects (grandchildren) Remarkably, reproductive dysfunction persists in the F2 generation despite the absence of direct EED exposure