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ABSTRACT
Acute alcohol feeding can activate autophagy and promotes the selection of autophagic vacuoles in the mitochondria, which is a key process regulating the occurrence and progression of alcohol steatohepatitis (ASH). In this study, ASH mice expressed more autophagy-associated proteins than healthy controls, as revealed by immunohistochemistry. In addition, transmission electron microscopy (TEM) detected a unique autophagy ultrastructure in ASH mouse liver cells, consisting of a large vesicle fused directly with mitochondria, which differed from the classical pattern. This novel type of mitophagy may provide a new avenue for a protective mechanism targeting mitophagy, which would benefit patients with ASH.
Abbreviations: ASH: alcoholic steatohepatitis; ALD: Alcoholic liver disease; ALT: alanine aminotransferase; AST: aspartate aminotransferase; HE: hematoxylin and eosin; TEM: transmission electron microscope; LC3: microtubule-associated protein 1 light chain 3; SQSTM1/p62: sequestosome 1; UQCRC2: ubiquinol-cytochrome c reductase core protein 2; PINK1: PTEN induced kinase 1; AMPK: AMP-activated protein kinase
Acknowledgments
The authors would like to thank Yili Sun and Cuiping Zhang for electron microscope technical guidance and assistance in this experiment. There are no conflicts of interest to declare.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Author contributions
Yanfei Lang: formal analysis, investigation, methodology and writing-original draft. Xiaxia Zhang: Methodology. Xin Li: software. Youqing Xu: conceptualization, data curation project administration, supervision and writing-review&editing. All authors approved the final version of the manuscript.