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Hepatocyte-specific IL11 cis-signaling drives lipotoxicity and underlies the transition from NAFLD to NASH

Nat Commun. 2021-01; 
Jinrui Dong, Sivakumar Viswanathan, Eleonora Adami, Brijesh K Singh, Sonia P Chothani, Benjamin Ng, Wei Wen Lim, Jin Zhou, Madhulika Tripathi, Nicole S J Ko, Shamini G Shekeran, Jessie Tan, Sze Yun Lim, Mao Wang, Pei Min Lio, Paul M Yen, Sebastian Schafer, Stuart A Cook, Anissa A Widjaja
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摘要

IL11 is important for fibrosis in non-alcoholic steatohepatitis (NASH) but its role beyond the stroma in liver disease is unclear. Here, we investigate the role of IL11 in hepatocyte lipotoxicity. Hepatocytes highly express IL11RA and secrete IL11 in response to lipid loading. Autocrine IL11 activity causes hepatocyte death through NOX4-derived ROS, activation of ERK, JNK and caspase-3, impaired mitochondrial function and reduced fatty acid oxidation. Paracrine IL11 activity stimulates hepatic stellate cells and causes fibrosis. In mouse models of NASH, hepatocyte-specific deletion of Il11ra1 protects against liver steatosis, fibrosis and inflammation while reducing serum glucose, cholesterol and triglyceride ... More

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