Open AccessEmerging Players in Autophagy Deficiency-Induced Liver Injury and Tumorigenesis
Author(s) -
Hua Yang,
HongMin Ni,
WenXing Ding
Publication year - 2019
Publication title -
gene expression
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 46
eISSN - 1555-3884
pISSN - 1052-2166
DOI - 10.3727/105221619x15486875608177
Subject(s) - autophagy , carcinogenesis , atg5 , liver injury , knockout mouse , cancer research , suppressor , microbiology and biotechnology , liver cancer , biology , cancer , endocrinology , genetics , gene , apoptosis , hepatocellular carcinoma
Studies using genetic mouse models that have defective autophagy have led to the conclusion that macroautophagy/autophagy serves as a tumor suppressor. One of such models is the liver-specific Atg5 or Atg7 knockout mice, and these knockout mice develop spontaneous liver tumors. It has been generally agreed that p62-mediated Nrf2 activation plays a critical role in promoting autophagy deficiency-induced liver injury and liver tumorigenesis. The mechanisms of how persistent Nrf2 activation induces liver injury and tumorigenesis are incompletely known. We discuss the recent progress on the new roles of HMGB1 and Yap in regulating liver injury and tumorigenesis in mice with liver-specific autophagy deficiency.