HCA2 activation confers neuroprotection in Parkinson’s disease models by suppressing oxidative stress and ferroptosis via the Nrf2/MGST1/GPX4 pathway

Key Points

• Neuroprotection is achieved through HCA2 activation, which suppresses oxidative stress and ferroptosis in Parkinson's disease models.
• Notably, activating HCA2 significantly reduces markers of oxidative stress and ferroptosis within these models.
• The study employs a combination of cellular and animal models to explore the Nrf2/MGST1/GPX4 signaling pathway.
• These findings indicate HCA2's potential role as a therapeutic target in addressing oxidative stress-related neuronal damage.