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.