The Emerging Role of Hepatocellular eNOS in Non-alcoholic Fatty Liver Disease Development

被引:16
作者
Cunningham, Rory P. [1 ,2 ]
Sheldon, Ryan D. [3 ]
Rector, R. Scott [1 ,2 ,4 ]
机构
[1] Harry S Truman Mem Vet Hosp, Res Serv, Columbia, MO 65201 USA
[2] Univ Missouri, Dept Nutr & Exercise Physiol, Columbia, MO 65211 USA
[3] Van Andel Inst, Metab & Nutr Programming, Ctr Canc & Cell Biol, Grand Rapids, MI USA
[4] Univ Missouri, Med, Div Gastroenterol & Hepatol, Columbia, MO 65211 USA
关键词
eNOS; nitric oxide; mitochondria; NAFLD; NASH; NITRIC-OXIDE SYNTHASE; ACTIVATED PROTEIN-KINASE; SINUSOIDAL ENDOTHELIAL-CELLS; MITOCHONDRIAL BIOGENESIS; V-PYRRO/NO; REGULATE AUTOPHAGY; INSULIN-RESISTANCE; OXIDATIVE STRESS; NATURAL-HISTORY; KNOCKOUT MICE;
D O I
10.3389/fphys.2020.00767
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
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.
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页数:9
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