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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.