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. 2020 Jun 12;10(16):7422–7435. doi: 10.7150/thno.42167

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Impact of hepatocyte-derived EVs on NAFLD under lipotoxicity. Hepatocytes tend to release EVs in response to toxic lipids, including PA and LPC. Lipotoxicity-induced EV release is dependent on TRAIL-R2 signaling, stress kinase MLK3, and ER stress sensor IRE1α. CXCL10 and ceramide-bearing EVs mediate monocyte/macrophage chemotaxis to hepatocytes while TRAIL-laden EVs activate macrophages. Vanin-1-enriched EVs can mediate endothelial cell migration, while miR-128-3p-bearing EVs contribute to the proliferation and activation of HSCs.