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Therefore, the major oxidative burst during I/R occurs after the reexposure to oxygen during the so called warm ischemia time.7 Although the molecular mechanisms involved in I/R cellular responses are still not fully understood, a major role seems to be played by APE/Ref-1 and NF-B proteins in liver.42 Overexpression of APE/Ref-1 by adenoviral vector resulted in suppression of the reperfusion-generated oxidative stress in a mouse model.42 Liver transplantation (LT) is at present the only available choice for the treatment of end-stage hepatic disease

Efficacy of N-methyl-D-aspartate receptor modulator augmentation in schizophrenia: A meta-analysis of randomised, placebo-controlled trials

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This effect is probably achieved through inhibiting Rb/E2F/c-myc and PI3K/AKT/mTOR signalling pathways [122]

Research has demonstrated that the liver has an iron-sensing function

Mechanisms and perspectives of sodium-glucose co-transporter 2 inhibitors in heart failure