HCA2 activation confers neuroprotection in Parkinson’s disease models by suppressing oxidative stress and ferroptosis via the Nrf2/MGST1/GPX4 pathway | Synapse
March 3, 2026
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.