Journal
DIGESTIVE DISEASES AND SCIENCES
Volume 61, Issue 5, Pages 1304-1313Publisher
SPRINGER
DOI: 10.1007/s10620-015-4025-x
Keywords
Autophagy; Insulin sensitivity; Liver injury; Nonalcoholic fatty liver disease; Oxidative stress; Steatosis
Categories
Funding
- NIH [R01DK061498, R01AA022601]
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Autophagy is a lysosomal degradative pathway that functions to promote cell survival by supplying energy in times of stress or by removing damaged organelles and proteins after injury. The involvement of autophagy in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) was first suggested by the finding that this pathway mediates the breakdown of intracellular lipids in hepatocytes and therefore may regulate the development of hepatic steatosis. Subsequent studies have demonstrated additional critical functions for autophagy in hepatocytes and other hepatic cell types such as macrophages and stellate cells that regulate insulin sensitivity, hepatocellular injury, innate immunity, fibrosis, and carcinogenesis. These findings suggest a number of possible mechanistic roles for autophagy in the development of NAFLD and progression to NASH and its complications. The functions of autophagy in the liver, together with findings of decreased hepatic autophagy in association with conditions that predispose to NAFLD such as obesity and aging, suggest that autophagy may be a novel therapeutic target in this disease.
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