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In recent years, the number of new mechanisms and molecular targets of SFN in the treatment of fatty liver reported by experimental studies has increased rapidly (Figure 1), such as inhibition of lipogenic enzymes via ER stress-dependent decrease of X-box binding protein 1 (XBP1) expression and ER stress-independent blocking of sterol regulatory element binding protein-1c (SREBP1c) pathways (Tian et al., 2018a), alleviated ER stress through the upregulation of AMPK and peroxisome proliferators-activated receptor (PPAR) (Mansour et al., 2022), enhanced mitochondrial function via Nrf2 activation or promotion of mitochondrial biogenesis by peroxisome proliferator-activated receptor alpha co-activator pathway (Lei et al., 2019), and regulation of FXR-mediated bile acid metabolism and LXR-mediated fatty acid synthesis pathways (Ma et al., 2022)

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43 : S45S53

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