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Reactive nitrogen species (RNS) such as nitric oxide promote damage to mitochondrial components, leading to dissipation of mitochondrial membrane potential and further increases in ROS and RNS production [42, 43]

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These results suggest that gpx4-dependent iron cell apoptosis may be targeted by blocking the Mtb ptpa- host PRMT6 interface, providing a new therapeutic strategy for the treatment of tuberculosis (145)