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

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

IL11 contributes to the development of non-alcoholic steatohepatitis (NASH) through incompletely understood mechanisms. Here, the authors report that lipotoxicity-driven autocrine IL11 activity underlies hepatocyte metabolic dysfunction and death via a NOX4/ERK-mediated mechanism while paracrine IL1...

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Main Authors: 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
Format: article
Language:EN
Published: Nature Portfolio 2021
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Science
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Online Access:https://doaj.org/article/ce2b5ee017d5453ea86274564e8eb24f
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Summary:IL11 contributes to the development of non-alcoholic steatohepatitis (NASH) through incompletely understood mechanisms. Here, the authors report that lipotoxicity-driven autocrine IL11 activity underlies hepatocyte metabolic dysfunction and death via a NOX4/ERK-mediated mechanism while paracrine IL11 activity stimulates hepatic stellate cells contributing to fibrosis and inflammation in the context of NASH.

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