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ROS acts as a central hub connecting ferroptosis to PCa pathogenesis, amplified by inflammatory signals and redox-sensitive transcription factors (e.g., Nrf2, HIF-1) that either directly enhance oxidative stress or indirectly modulate ferroptosis susceptibility [Figure 2A]

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111-148) was enacted, followed by enactment of the Health Care and Education Reconciliation Act of 2010 (Pub