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This oxidative burden is exacerbated by Ang II, which promotes mitochondrial fission via dynamin-related protein 1 (Drp1) and inhibits mitophagy, leading to the accumulation of damaged, ROS-producing mitochondria (Tábara et al., 2025)

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As newly identified metal ion-dependent programmed cell death modalities, ferroptosis and cuproptosis play critical roles in tumor metabolism, immune microenvironment remodeling, and therapeutic resistance, representing emerging research foci in OSCC