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Mitochondrial dysfunction compromises the energy supply of ATP to neurons, calcium homeostasis and leads to high levels of ROS that accelerate the mutation rate of mitochondrial DNA (mtDNA) and lipoperoxidation of neuronal membranes, causing decomposition of PUFAs and the formation of highly reactive end products: malondialdehyde (MDA) and 4-hydroxy-2-nonenal (HNE) (the most toxic species related to cell damage and apoptosis) (Petrozzi et al., 2007
Proteasome inhibitor-induced apoptosis in CLL is associated with immediate disruption of mitochondrial function
Here, we show the necessity of adenosine A2A receptor (A2AR) signaling and the GSH/GPX4 axis in orchestrating metabolic fitness and survival of functionally competent CD8 + T cells
These side effects are usually mild and may get better over time
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