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Abstract Details
The Emerging Role of Hepatocellular eNOS in Non-alcoholic Fatty Liver Disease Development
Rory P Cunningham12, Ryan D Sheldon3, R Scott Rector124
Author information
1Research Service, Harry S. Truman Memorial Veterans' Hospital, Columbia, MO, United States.
2Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO, United States.
3Metabolic and Nutritional Programming, Center for Cancer and Cell Biology, Van Andel Institute, Grand Rapids, MI, United States.
4Medicine-Division of Gastroenterology and Hepatology, University of Missouri, Columbia, MO, United States.
Abstract
Non-alcoholic fatty liver disease (NAFLD) is comprised of a spectrum of liver injury ranging from excess fat accumulation in the liver (steatosis), to steatohepatitis (NASH), to its end stage of cirrhosis. A hallmark of NAFLD progression is the decline in function of hepatic mitochondria, although the mechanisms remain unresolved. Given the important role endothelial nitric oxide synthase (eNOS) plays in mitochondrial dynamics in other tissues, it has emerged as a potential mediator of maintaining mitochondrial function in the liver. In this mini review, we summarize the most relevant findings that extends current understanding of eNOS as a regulator of mitochondrial biogenesis, and identifies a potential additional role in mitochondrial turnover and attenuating inflammation during NAFLD development and progression.