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DXR increases the generation of reactive oxygen species (ROS) and weakens enzymatic and non-enzymatic antioxidant defense systems (5).Contemporary studies have demonstrated the involvement of endoplasmic reticulum (ER) stress in DXRinduced cardiotoxicity (6).ER stress is a condition arising from disruptions in ER functions due to various stressors, including adenosine triphosphate deficiency, oxidative stress, drugs, or toxins, and if it persists for a prolonged period, it can lead to cell death (7).In DXR-induced cardiotoxicity, the upregulation of ER stress proteins, including glucose-regulated protein (GRP)78, as well as caspase-12 activation have been reported previously (8,9).
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Cırrık et al. (2024) studied this question.
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