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To better understand the mechanism of HO-1 action in VaD and its potential therapeutic value, future investigations should be directed toward the following objectives: (1) clarifying the specific mechanisms of HO-1-derived metabolites and comparing their effects across various disease models

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Abstract Glucose-6-phosphate dehydrogenase (G6PD) deficiency, one of the most common human genetic enzymopathies, is caused by over 160 different point mutations and contributes to the severity of many acute and chronic diseases associated with oxidative stress, including hemolytic anemia and bilirubin-induced neurological damage particularly in newborns