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Fisetin attenuates doxorubicin-induced cardiomyopathy and by inhibiting ferroptosis through SIRT1/Nrf2 signaling pathway activation

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[1, 2, 3, 4] Despite extensive research, the precise cellular and molecular mechanisms that drive the pathogenesis of those conditions are only partly understood, with a resulting variety of therapeutic approaches that depend on the symptoms, signs, and stage of the disease

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Research has explored its activity in glucose metabolism, insulin signaling pathways, and mitochondrial function in controlled laboratory environments