Although the release of these proteins into the cytosol is expected to trigger apoptosis, this form of cell death is negligible in APAP-induced hepatotoxicity, as shown by the absence of caspases activation and the inability of caspase inhibitors to protect against APAP-induced liver injury ( in vitro after treatment with APAP and fructose, which acts as a glycolytic substrate to generate ATP and glycine as a membrane stabilizer ( As MPT and JNK are key players in APAP-mediated acute liver failure, it is unclear whether mitochondrial dysfunction and JNK are engaged in low dose APAP exposure without liver injury
Disrupted skeletal muscle mitochondrial dynamics, mitophagy, and biogenesis during cancer cachexia: a role for inflammation
PLoS One 12(11):e0187351 Zmock M, Hofbauer S, Schaffner I, Gasselhuber B, Nicolussi A, Soudi M, Pirker KF, Furtmller PG, Obinger C (2015) Independent evolution of four heme peroxidase superfamilies

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