Proposed possible molecular and cellular scenarios on how p62 regulates the formation of MDBs and SGs in alcohol-induced liver injury. (IMAGE)
Caption
(A) Chronic plus binge alcohol feeding impairs hepatic lysosomal biogenesis, leading to insufficient autophagy, which leads to increased hepatic p62 accumulation. Increased hepatic p62 promotes the formation of MDBs and SGs but is dispensable for the selective autophagic clearance of MDBs and SGs. (B) DDC increases hepatic MDB but not SG formation. DDC may also activate hepatic autophagy to promote its clearance. In this DDC alone condition, p62 is dispensable for both MBD and SG formation. (C) Alcohol feeding in post-DDC treatment may impair hepatic autophagy leading to increased hepatic p62 accumulation. Increased hepatic p62 promotes the formation of MDBs but not SGs. p62 is dispensable for the selective autophagic clearance of MDBs and SGs, similar to scenario A. Created with BioRender.com. ALD, alcohol-associated liver disease; DDC, 3,5-diethoxycarbonyl-1,4-dihydrocollidine; MDB, Mallory-Denk body; SG, stress granule.
Credit
By Wen-Xing Ding, Hong-Min Ni, Zhaoli Sun, et al.
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CC BY-NC