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Its mechanism centers on mitochondrial lipoylated protein aggregation and Fe-S cluster protein inactivation, yet it also exhibits cross-talk with other cell death pathways

Furthermore, Fe 2+ can exit cells through exosomes or undergo re-oxidation to Fe 3+ via ferric oxidases like ceruloplasmin or hephaestin (Torti and Torti, 2013

Transcriptional regulation and multiple functions of MAO genes

Kleinschnitz C, Grund H, Wingler K, Armitage ME, Jones E, Mittal M, Barit D et al (2010) Post-stroke inhibition of induced NADPH oxidase type 4 prevents oxidative stress and neurodegeneration

Zembowicz A, Hatchett RJ, Radziszewski W, Gryglewski RJ