Cunningham Rory P, Sheldon Ryan D, Rector R Scott
Research Service, Harry S. Truman Memorial Veterans' Hospital, Columbia, MO, United States.
Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO, United States.
Front Physiol. 2020 Jul 3;11:767. doi: 10.3389/fphys.2020.00767. eCollection 2020.
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.
非酒精性脂肪性肝病（NAFLD）包括一系列肝脏损伤，从肝脏中脂肪过度积累（脂肪变性）到脂肪性肝炎（NASH），再到其终末期肝硬化。NAFLD进展的一个标志是肝线粒体功能下降，尽管其机制仍未明确。鉴于内皮型一氧化氮合酶（eNOS）在其他组织的线粒体动力学中发挥重要作用，它已成为维持肝脏线粒体功能的潜在介质。在本综述中，我们总结了最相关的研究结果，这些结果扩展了目前对eNOS作为线粒体生物发生调节因子的理解，并确定了其在NAFLD发生和发展过程中线粒体更新及减轻炎症方面可能的额外作用。
