Rubicon inhibits autophagy and accelerates hepatocyte apoptosis and lipid accumulation in nonalcoholic fatty liver disease in mice.

Satoshi TanakaHayato HikitaTomohide TatsumiRyotaro SakamoriYasutoshi NozakiSadatsugu SakaneYuto ShiodeTasuku NakaboriYoshinobu SaitoNaoki HiramatsuKeisuke TabataTsuyoshi KawabataMaho HamasakiHidetoshi EguchiHiroaki NaganoTamotsu YoshimoriTetsuo Takehara

Published in: Hepatology (Baltimore, Md.) (2016)

Rubicon is overexpressed and plays a pathogenic role in NAFLD by accelerating hepatocellular lipoapoptosis and lipid accumulation, as well as inhibiting autophagy. Rubicon may be a novel therapeutic target for regulating NAFLD development and progression. (Hepatology 2016;64:1994-2014).

Keyphrases

endoplasmic reticulum stress
cell death
oxidative stress
signaling pathway
cell cycle arrest
liver injury
metabolic syndrome
adipose tissue
cell proliferation
wild type