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Treating mice with acivicin, which enhances antioxidant capacity by inhibiting glutathione breakdown, reduced oxidative damage and neurodegeneration even 80 days post-disease onset, highlighting the therapeutic potential of targeting ROS production ( Liu and colleagues used a cuprizone-induced demyelination model in adult male mice to investigate Hv1 in demyelination ( Wang and colleagues further investigated Hv1 in microglial migration and myelin debris clearance ( in vivo , however, the ability of the reported anti-Hv1 antibody to block proton channel activity warrants further investigation

J Hepatol 2008

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