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. 2023 Feb 25;14(2):160. doi: 10.1038/s41419-023-05669-4

Table 2.

Roles of SESN2 in hepatic fibrosis and cirrhosis.

Study subjects/Model SESN2 expression Intervention HSCs activation and α-SMA expression Overall outcome Reference
mRNA protein
In vitro models Primary HSCs isolated from CCl4‐treated mice No data Increased No data No data No data [103]
Auto-activated primary HSCs from healthy wild-type mice Increased Increased No data No data No data [103]
LX-2 cells treated with TGF-β for no more than 12 h Increased Increased Plasmid-mediated SESN2 overexpression Decreased No data [103]
HSC-T6 cells treated with TGF-β for 48 h Decreased Decreased Plasmid-mediated SESN2 overexpression Decreased No data [102]
In vivo models Mice fed with HFD for induction of non-alcoholic fatty liver fibrosis No data Increased SESN2 knockout Increased SESN2 ablation provokes HSCs activation, collagen production, and hepatic fibrogenesis. [60]
Mice injected with CCl4 or received BDL for induction of hepatic fibrosis No data Decreased Adenoviral or lentiviral expression of SESN2 Decreased Exogenous SESN2 expression contributes to decreased serum ALT and AST activities, inflammatory cell infiltration, and hepatic collagen deposition. [102, 103]
Clinical samples Cirrhotic liver tissues Decreased Decreased No data No data SESN2 expression is decreased in cirrhotic livers and negatively correlated with disease progression. [103]

ALT alanine aminotransferase, AST aspartate aminotransferase, α-SMA alpha smooth muscle actin, BDL bile duct ligation, CCl4 carbon tetrachloride, HFD high-fat diet, HSCs hepatic stellate cells, SESN2 Sestrin2, TGF-β transforming growth factor beta.