When SETD1B is functional, mycolactone exposure leads to the upregulation of CHAC1, resulting in decreased GSH levels and increased oxidative stress, ultimately causing apoptosis
Amino acid signature during sickle cell pain crisis shows significant alterations related to nitric oxide and energy metabolism
Interestingly, the categories enriched in the upregulated clusters are related to phagosome maturation, RNA and translation, but importantly multiple metabolism pathways including citric acid cycle, cholesterol metabolism, pentose phosphate pathway, electron transport chain, and glutathione metabolism
[4] [14] This depletion may result from increased oxidative stress, inflammation, and the metabolic burden placed on the liver by excess fat accumulation
K., et al., [Effect of carnosine and -lipoic acid on hepatocyte apoptosis and the cytokine profile in induced fatty liver disease in Wistar rats]