title: [Effect of autophagy on liver regeneration].
abstract: Autophagy is a lysosome-mediated degradation pathway, which plays an important role in hepatic physiological and pathological processes, in eukaryotic cells. The liver has a remarkable regenerative capacity. After acute or chronic injury, the residual hepatic cells can be activated to enter the cell-cycle for proliferation, in order to compensate for lost liver tissue and recover liver function. In this review, we summarize the relationship between liver regeneration (LR) after various types of injury and autophagy. For example, autophagy is activated to accelerate LR after physically, alcohol and food borne induced liver injury, while the role of autophagy in animal models of LR after chemical injury remains controversial. Autophagy can also be used to promote the replication of virus particles by some hepatotropic viruses (e.g., HBV, HCV) and inhibit LR after viral infection. Studies on mechanisms of autophagy and LR will contribute to clarify the regenerative process and provide new methods for the treatment of liver disease.
authors.affiliation: 1. State Key Laboratory Cultivation Base for Cell Differentiation Regulation, College of Life Science, Henan Normal University, Xinxiang 453007, China; 2. Henan Bioengineering Key Laboratory, Henan Normal University, Xinxiang 453007, China; 3. Henan Engineering Laboratory for Bioengineering and Drug Development, Henan Normal University, Xinxiang 453007, China;
authors.forename: Qi-wen
authors.initials: QW
authors.lastname: Wang
authors.affiliation: 1. State Key Laboratory Cultivation Base for Cell Differentiation Regulation, College of Life Science, Henan Normal University, Xinxiang 453007, China; 2. Henan Bioengineering Key Laboratory, Henan Normal University, Xinxiang 453007, China; 3. Henan Engineering Laboratory for Bioengineering and Drug Development, Henan Normal University, Xinxiang 453007, China;
authors.forename: Cui-fang
authors.initials: CF
authors.lastname: Chang
authors.affiliation: 1. State Key Laboratory Cultivation Base for Cell Differentiation Regulation, College of Life Science, Henan Normal University, Xinxiang 453007, China; 2. Henan Bioengineering Key Laboratory, Henan Normal University, Xinxiang 453007, China; 3. Henan Engineering Laboratory for Bioengineering and Drug Development, Henan Normal University, Xinxiang 453007, China;
authors.forename: Ning-ning
authors.initials: NN
authors.lastname: Gu
authors.affiliation: 1. State Key Laboratory Cultivation Base for Cell Differentiation Regulation, College of Life Science, Henan Normal University, Xinxiang 453007, China; 2. Henan Bioengineering Key Laboratory, Henan Normal University, Xinxiang 453007, China; 3. Henan Engineering Laboratory for Bioengineering and Drug Development, Henan Normal University, Xinxiang 453007, China;
authors.forename: Cui-yun
authors.initials: CY
authors.lastname: Pan
authors.affiliation: 1. State Key Laboratory Cultivation Base for Cell Differentiation Regulation, College of Life Science, Henan Normal University, Xinxiang 453007, China; 2. Henan Bioengineering Key Laboratory, Henan Normal University, Xinxiang 453007, China; 3. Henan Engineering Laboratory for Bioengineering and Drug Development, Henan Normal University, Xinxiang 453007, China;
authors.forename: Cun-shuan
authors.initials: CS
authors.lastname: Xu
mesh_terms: D000818:Animals; D001343:Autophagy; D056486:Chemical and Drug Induced Liver Injury / Q000503:physiopathology; D006509:Hepatitis B / Q000503:physiopathology; D006526:Hepatitis C / Q000503:physiopathology; D006801:Humans; D008115:Liver Regeneration