Progress of Heme Oxygenase-1 Mediated Ferroptosis in Non-alcoholic Fatty Liver Disease

Abstract

Ferroptosis plays an important role in the progression of non-alcoholic fatty liver disease (NAFLD) as a novel mode of programmed cell death. Heme oxygenase-1 (HO-1), acting as an inducible oxidase, has been shown the capability of alleviating oxidative stress and hepatocyte necrosis to prevent or delay the progression of NAFLD. However, the mechanism of HO-1 regulating ferroptosis and affecting the development of NAFLD remains inadequately explored. This review provided a systematic and comprehensive summary of the effects of HO-1 on NAFLD by regulating ferroptosis, and discussed the mechanism of HO-1 in preventing the development of NAFLD by summarizing the relevant literature in recent years, and showed that HO-1 regulates ferroptosis in NAFLD through the generation of antioxidants (such as bilirubin and CO), activation of the System Xc, and facilitation of ferrous ion accumulation, in order to provide a theoretical basis for targeting HO-1 gene therapy for NAFLD by methods such as pharmacological interventions and provide a reference for further research.

Keywords

• non-alcoholic fatty liver disease|heme oxygenase-1|ferroptosis|review