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Notably, metabolically activated ATMs express lysosome-associated programs, promote inflammation, and participate in the clearance of dead adipocytes through lysosomal exocytosis, highlighting that ATMs responses to obesity reflect specialized adaptations to lipid-rich, damaged tissue environments rather than a simple shift between canonical activation states (114)

However, excessive PARP1 activation, due to exposure to genotoxic agents, can dramatically reduce NAD + and ATP levels, affecting sirtuin activity and cellular homeostasis and leading to cell death

Lill and Freibert, 2020) have observed biochemical and morphological characteristics of ferroptosis in the brains of AD patients or mice, including iron metabolism imbalance, glutathione (GSH) degradation, inactivation of glutathione peroxidase 4 (GPX4) leading to increased reactive oxygen species (ROS), lipid peroxidation, and mitochondrial abnormalities

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