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
Study subjects/Model		mRNA	protein	Intervention	HSCs activation and α-SMA expression	Overall outcome	Reference
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]
In vivo models	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.

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