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. Author manuscript; available in PMC: 2022 Oct 21.
Published in final edited form as: Mol Aspects Med. 2021 Jun 11;82:100973. doi: 10.1016/j.mam.2021.100973

Fig. 6. Various HCC risk factors impair hepatic autophagy.

Fig. 6.

Activation of oncogenes or loss of tumor suppressor genes (such as tsc1 or pten) causes mTORC1 activation. NAFLD and AALD impair TFEB-mediated lysosomal biogenesis and decrease autophagy proteins such as ATG7. Both HBV and HCV infection either impairs lysosomal function or inhibits fusion of autophagosomes with lysosomes, leading to autophagy inhibition or delayed autophagic flux. All these primary risk factors for chronic liver diseases thus lead to inhibition of hepatic autophagy. Impaired hepatic autophagy increased accumulation of damaged mitochondrial, oxidative stress, genomic instability and non-canonical p62-Keap1-Nrf2 activation, ultimately resulting in liver cancer.