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Therapeutic effects of the mitochondrial ROS-redox modulator KH176 in a mammalian model of Leigh Disease

In an animal model of AD expressing ABCC1, the activation of this protein substantially decreased the accumulation of A (231)

Research indicates that mitochondrial GPX4 depletion increases ROS, further contributing to cellular damage and ferroptosis (Agrawal et al., 2018)

Depletion of MPST also increased radical load, albeit to a lesser extent than depletion of CSE (Extended Data Fig
