Host homeostatic responses to alcohol-induced cellular stress in animal models of alcoholic liver disease

2015 ◽  
Vol 9 (9) ◽  
pp. 1193-1205
Author(s):  
He Joe Wang ◽  
Gary J Murray ◽  
Mary Katherine Jung
Keyword(s):  
Liver Disease ◽  
Animal Models ◽  
Alcoholic Liver Disease ◽  
Cellular Stress

scholarly journals Pathogenesis and Management of Alcoholic Liver Disease

2016 ◽  
Vol 34 (4) ◽  
pp. 347-355 ◽  
Author(s):  
M. Omar Farooq ◽  
Ramon Bataller
Keyword(s):  
Liver Disease ◽  
Animal Models ◽  
Alcoholic Liver Disease ◽  
Disease Stage ◽  
Human Samples ◽  
Pathogenic Factors ◽  
Alcohol Abstinence ◽  
Current Therapies ◽  
Advanced Stages ◽  
Translational Studies

Alcoholic liver disease (ALD) is a leading cause of liver-related morbidity and mortality. ALD encompasses a spectrum of disorders ranging from asymptomatic steatosis, alcoholic steatohepatitis, fibrosis, cirrhosis and its related complications. Moreover, patients can develop an acute-on-chronic form of liver failure called alcoholic hepatitis (AH). Most patients are diagnosed at advanced stages of the disease with higher rates of complications and mortality. The mainstream of therapy of ALD patients, regardless of the disease stage, is prolonged alcohol abstinence. The current therapeutic regimens for AH (i.e. prednisolone) have limited efficacy and targeted therapies are urgently needed. The development of such therapies requires translational studies in human samples and suitable animal models that reproduce clinical and histological features of AH. In recent years, new animal models that simulate some of the features of human AH have been developed, and translational studies using human samples have identified potential pathogenic factors and histological parameters that predict survival. In this review, we discuss the pathogenesis and management of ALD, focusing on AH, its current therapies and potential treatment targets.

scholarly journals Alcoholic liver disease: Utility of animal models

2018 ◽  
Vol 24 (45) ◽  
pp. 5063-5075 ◽  
Author(s):  
Arantza Lamas-Paz ◽  
Fengjie Hao ◽  
Leonard J Nelson ◽  
Maria Teresa Vázquez ◽  
Santiago Canals ◽  
...  
Keyword(s):  
Liver Disease ◽  
Animal Models ◽  
Alcoholic Liver Disease

Alcoholic liver disease and exacerbation by malnutrition and infections: what animal models are currently available?

2010 ◽  
Vol 1216 (1) ◽  
pp. 41-49 ◽  
Author(s):  
Ina Bergheim ◽  
Patricia K. Eagon ◽  
Steven Dooley ◽  
Katja Breitkopf-Heinlein
Keyword(s):  
Liver Disease ◽  
Animal Models ◽  
Alcoholic Liver Disease

Animal models for alcoholic liver disease

Hepatology ◽  
1989 ◽  
Vol 9 (6) ◽  
pp. 904-905 ◽  
Author(s):  
Esteban Mezey
Keyword(s):  
Liver Disease ◽  
Animal Models ◽  
Alcoholic Liver Disease

scholarly journals Animal Models of Alcoholic Liver Disease: Pathogenesis and Clinical Relevance

2017 ◽  
Vol 17 (3) ◽  
pp. 173-186 ◽  
Author(s):  
Bin Gao ◽  
Ming-Jiang Xu ◽  
Adeline Bertola ◽  
Hua Wang ◽  
Zhou Zhou ◽  
...  
Keyword(s):  
Liver Disease ◽  
Animal Models ◽  
Alcoholic Liver Disease ◽  
Clinical Relevance ◽  
Disease Pathogenesis

Early-Phase Alcoholic Liver Disease: An Update on Animal Models, Pathology, and Pathogenesis

2004 ◽  
Vol 23 (4) ◽  
pp. 217-231 ◽  
Author(s):  
Shashi K. Ramaiah ◽  
Chantal Rivera ◽  
Gavin E. Arteel
Keyword(s):  
Liver Disease ◽  
Animal Models ◽  
Alcoholic Liver Disease ◽  
Early Phase ◽  
Morbidity And Mortality ◽  
Alcohol Metabolism ◽  
Pathologic Findings ◽  
Common Etiology ◽  
Insight Into

Alcoholic liver disease (ALD) remains to be one of the most common etiology of liver disease and is a major cause of morbidity and mortality worldwide. The pathologic stages of ALD comprises of steatosis, steatohepatitis, and fibrosis/cirrhosis. Steatosis and steatohepatitis represents the early phase of ALD and are precursor stages for fibrosis/cirrhosis. Numerous research efforts have been directed at recognizing cofactors interacting with alcohol in the pathogenesis of steatosis and steatohepatitis. This review will elucidate the constellation of complex pathogenesis, available animal models, and microscopic pathologic findings mostly in the early-phase of ALD. The role of endotoxin, reactive oxygen species, alcohol metabolism, and cytokines are discussed. Understanding the mechanisms of early-phase ALD should provide insight into the development of therapeutic strategies and thereby decrease the morbidity and mortality associated with ALD.

scholarly journals Animal Models of Alcoholic Liver Disease

2010 ◽  
Vol 28 (6) ◽  
pp. 729-736 ◽  
Author(s):  
Gavin E. Arteel
Keyword(s):  
Liver Disease ◽  
Animal Models ◽  
Alcoholic Liver Disease

scholarly journals Animal Models of Alcoholic Liver Disease for Hepatoprotective Activity Evaluation

2021 ◽  
Vol 41 ◽  
pp. 07007
Author(s):  
Hidayah Dwi Renggani ◽  
Triana Hertianti ◽  
Retno Murwanti
Keyword(s):  
Liver Disease ◽  
Animal Models ◽  
Liver Injury ◽  
Alcoholic Liver Disease ◽  
Hepatoprotective Activity ◽  
Chronic Ethanol ◽  
Injury Model ◽  
Acute Ethanol ◽  
Injury Models ◽  
Hepatoprotective Agents

Background: The reported statistics suggest that alcoholic liver disease is on the rise. Furthermore, medications used to treat the disease have unpleasant effects, and this necessitates the need to continuously investigate hepatoprotective agents. This study investigates animal models of alcoholic liver disease used to evaluate hepatoprotective activity. Content: A good number of published articles evaluating hepatoprotective activity were summarized. The studies used three ethanol-induced liver injury models: the acute ethanol-induced liver injury model, the chronic ethanol-induced liver injury model, and Lieber– DeCarli model. Summary: Wistar rats were primarily used in the ethanol-induced liver injury model. High levels of alanine transaminase (ALT) and aspartate transaminase (AST) and histopathological alterations were found in all animal models (acute ethanol-induced liver injury, chronic ethanol-induced liver injury, and Lieber–DeCarli models). Severe steatosis was shown in both chronic ethanol-induced liver injury and Lieber–DeCarli models. However, fibrosis was undetected in all models.

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