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This combination triggers potent inflammatory stimuli via macrophage and neutrophil activation and accompanying release of pro-inflammatory cytokines (93, 9597)

Pro-apoptotic complexes of BAX and BAK on the outer mitochondrial membrane

To this end, we created a mouse model, which combined genetically encoded chronic mitochondrial oxidative stress due to Sod2 haploinsufficiency with genomic prkn deficiency

This shift leads to an increase in reactive oxygen species (ROS) production and depletes glutathione (GSH), a crucial antioxidant in hepatocytes (Chen et al ., 2018)

[Abstract]2024 Feb 21;22(1):192

10.1002/bit.28606 2 AdlimoghaddamA.NeuendorffM.RoyB.AlbensiB