Hepatocyte-specific IL11 cis-signaling drives lipotoxicity and underlies the transition from NAFLD to NASH
Jinrui Dong; Sivakumar Viswanathan; Eleonora Adami; Brijesh Kumar Singh; Sonia Chothani; Benjamin Ng; Wei‐Wen Lim; Jin Zhou · 2021 · Nature Communications
WASTE classifies this as Negative / Null Result Report · AI classification, approximate
The study found no significant effect — useful as a negative control or null benchmark for your own design.
Abstract
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
Abstract by Jinrui Dong; Sivakumar Viswanathan; Eleonora Adami; Brijesh Kumar Singh; Sonia Chothani; Benjamin Ng; Wei‐Wen Lim; Jin Zhou, Nature Communications (2021) — licensed CC BY 4.0.
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Metadata source: OpenAlex · DOI 10.1038/s41467-020-20303-z