|  Help  |  About  |  Contact Us

Publication : Diverse Consequences in Liver Injury in Mice with Different Autophagy Functional Status Treated with Alcohol.

First Author  Yan S Year  2019
Journal  Am J Pathol Volume  189
Issue  9 Pages  1744-1762
PubMed ID  31199920 Mgi Jnum  J:282111
Mgi Id  MGI:6369883 Doi  10.1016/j.ajpath.2019.05.011
Citation  Yan S, et al. (2019) Diverse Consequences in Liver Injury in Mice with Different Autophagy Functional Status Treated with Alcohol. Am J Pathol 189(9):1744-1762
abstractText  Alcoholic fatty liver disease is often complicated by other pathologic insults, such as viral infection or high-fat diet. Autophagy plays a homeostatic role in the liver but can be compromised by alcohol, high-fat diet, or viral infection, which in turn affects the disease process caused by these etiologies. To understand the full impact of autophagy modulation on alcohol-induced liver injury, several genetic models of autophagy deficiency, which have different levels of functional alterations, were examined after acute binge or chronic-plus-binge treatment. Mice given alcohol with either mode and induced with deficiency in liver-specific Atg7 shortly after the induction of Atg7 deletion had elevated liver injury, indicating the protective role of autophagy. Constitutive hepatic Atg7-deficient mice, in which Atg7 was deleted in embryos, were more susceptible with chronic-plus-binge but not with acute alcohol treatment. Constitutive hepatic Atg5-deficient mice, in which Atg5 was deleted in embryos, were more susceptible with acute alcohol treatment, but liver injury was unexpectedly improved with the chronic-plus-binge regimen. A prolonged autophagy deficiency may complicate the hepatic response to alcohol treatment, likely in part due to endogenous liver injury. The complexity of the relationship between autophagy deficiency and alcohol-induced liver injury can thus be affected by the timing of autophagy dysfunction, the exact autophagy gene being affected, and the alcohol treatment regimen.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

5 Authors

9 Bio Entities

0 Expression