Senescence and cell death in chronic liver injury: roles and mechanisms underlying hepatocarcinogenesis
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Mengchao Xiao1,*, Wenjian Chen1,*, Chao Wang1,*, Yingfu Wu1, Shiwei Zhu1, Chuyang Zeng1, Yongchao Cai2, Changcheng Liu2 and Zhiying He1,2
1Department of Cell Biology, Center for Stem Cell and Medicine, Second Military Medical University, Shanghai, China
2Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China
*These authors contributed equally to this work
Zhiying He, email: email@example.com
Keywords: chronic liver injury; senescence; apoptosis; necroptosis; necrosis
Received: August 24, 2017 Accepted: November 10, 2017 Published: December 22, 2017
Chronic liver injury (CLI) is a complex pathological process typically characterized by progressive destruction and regeneration of liver parenchymal cells due to diverse risk factors such as alcohol abuse, drug toxicity, viral infection, and genetic metabolic disorders. When the damage to hepatocytes is mild, the liver can regenerate itself and restore to the normal state; when the damage is irreparable, hepatocytes would undergo senescence or various forms of death including apoptosis, necrosis and necroptosis. These pathological changes not only promote the progression of the existing hepatopathies via various underlying mechanisms but are closely associated with hepatocarcinogenesis. In this review, we discuss the pathological changes that hepatocytes undergo during CLI, and their roles and mechanisms in the progression of hepatopathies and hepatocarcinogenesis. We also give a brief introduction about some animal models currently used for the research of CLI and progress in the research of CLI.
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