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AUTHOR'S VIEW

TAK1-dependent autophagy: A suppressor of fatty liver disease and hepatic oncogenesis

Article: e968507 | Received 19 Aug 2014, Accepted 20 Aug 2014, Published online: 31 Dec 2014

Figures & data

Figure 1. TAK1-mediated autophagy prevents hepatic steatosis and tumorigenesis. Upon nutrition deprivation, TGF-β activated kinase 1 (TAK1) mediates autophagy through activation of AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin complex 1 (mTORC1). TAK1 is also associated with induction of peroxisome proliferator-activated receptor (PPAR) α-mediated fatty acid oxidation (FAO) through suppression of mTORC1. Both autophagy and FAO contribute to lipid breakdown to prevent excessive lipid accumulation in hepatocytes. Autophagy prevents, and mTORC1 enhances, spontaneous tumorigenesis in the liver.

Figure 1. TAK1-mediated autophagy prevents hepatic steatosis and tumorigenesis. Upon nutrition deprivation, TGF-β activated kinase 1 (TAK1) mediates autophagy through activation of AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin complex 1 (mTORC1). TAK1 is also associated with induction of peroxisome proliferator-activated receptor (PPAR) α-mediated fatty acid oxidation (FAO) through suppression of mTORC1. Both autophagy and FAO contribute to lipid breakdown to prevent excessive lipid accumulation in hepatocytes. Autophagy prevents, and mTORC1 enhances, spontaneous tumorigenesis in the liver.