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Notably, GSH acts as a critical antioxidant that protects cancer cells from any form of programmed cell death (i.e., autophagy, apoptosis, necroptosis, and ferroptosis) 50,51,52

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]