Hepatic stellate cells (HSC) are the key fibrogenic cells of the liver. HSC activation is a process of cellular transdifferentiation that occurs upon liver injury, but the mechanisms underlying liver fibrosis are unknown. Nuclear erythroid 2-related factor 2 (Nrf2) is an oxidative stress-mediated transcription factor with a variety of downstream targets aimed at cytoprotection. However, Nrf2 has recently been implicated as a new therapeutic target for the treatment of liver fibrosis. This review focuses on the transcriptional repressors that either control liver injury or regulate specific fibrogenic functions of liver fibrosis. We also show that Nrf2 may reveal significant gene expression changes, suggesting that Nrf2 activation may ameliorate liver fibrosis.
Keywords: APAP; ARE; ECM; EGF; ERK; Extracellular signal-regulated kinase; HCC; HO-1; HSC; Hepatic stellate cell; ITC; KEAP1; Liver fibrosis; MAPK; NASH; NF-κB; NOTCH 1; Notch homolog 1; Nrf2; Nuclear erythroid 2-related factor 2; Oxidative stress; PCP; PDGF; PERK; PI3K; PKC; PKR-like endoplasmic reticulum kinase; Pentachlorophenol; Phosphoinositide 3-kinase inhibitor; RNS; ROS; TBARs; TGF-β1; acetaminophen; antioxidant response element; epidermal growth factor; extracellular matrix; heme oxygenase-1; hepatic stellate cells; hepatocellular carcinoma; isothiocyanates; kelch-like ECH-associated protein 1; mTOR; mammalian target of rapamycin; mitogen-activated protein kinase; nonalcoholic steatohepatitis; nuclear erythroid 2-related factor 2; nuclear factor-κB; platelet-derived growth factor; protein kinase C; reactive nitrogen species; reactive oxygen species; thiobarbituric- acid-reactive substances; transforming growth factor-β1; α-SMA; α-smooth muscle actin.
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