Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
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.
The mechanisms underlying the transmission of Tau in astrocytes are unclear. Here, the authors show that the entry of filamentous recombinant human Tau into astrocytes via the integrin αV/ β1 complex stimulates integrin signaling, resulting in activation of NFκB and astrocyte conversion towards a neurotoxic state.
