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This paper reviews the Met metabolism in normal conditions and its dysregulation under abnormal conditions, the possible causes of hypermethioninemia, and its connection to BA pathogenesis: Abnormal hepatic level of Met could lead to a perturbation of redox homeostasis and mitochondrial functions of hepatocytes, enhancement of viral infectivity, and dysregulation of innate and adaptative immune cells in response to infection/damage of the liver contributing to the initiation/progression of BA
Brain-related diseases The pathophysiological process of hypoxic-ischemic (HI) brain injury involves multiple mechanisms, including synaptic injury, 252 inflammation, 253 and oxidative stress
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