The pathogenesis and molecular pathways involved in non-alcoholic fatty liver disease (NAFLD) are reviewed, as well as what is known about mitochondrial dysfunction that leads to heart disease and the progression to steatohepatitis and hepatic fibrosis. We focused our discussion on the role of the antioxidant gene heme oxygenase-1 (HO-1) and its nuclear coactivator, peroxisome proliferator-activated receptor-gamma coactivator (PGC1-α) in the regulation of mitochondrial biogenesis and function and potential therapeutic benefit for cardiac disease, NAFLD as well as the pharmacological effect they have on the chronic inflammatory state of obesity. The result is increased mitochondrial function and the conversion of white adipocyte tissue to beige adipose tissue (“browning of white adipose tissue”) that leads to an improvement in signaling pathways and overall liver function. Improved mitochondrial biogenesis and function is essential to preventing the progression of hepatic steatosis to NASH and cirrhosis as well as preventing cardiovascular complications.

回顾了非酒精性脂肪肝疾病（NAFLD）的发病机理和分子途径，以及关于导致心脏病以及发展为脂肪性肝炎和肝纤维化的线粒体功能障碍的已知知识。我们集中讨论了抗氧化剂基因血红素加氧酶-1（HO-1）及其核辅激活因子，过氧化物酶体增殖物激活受体-γ辅激活因子（PGC1-α）在调节线粒体生物发生和功能以及潜在治疗益处中的作用。对于心脏病，NAFLD及其对肥胖症慢性炎症状态的药理作用。结果是线粒体功能增强，白色脂肪细胞组织转变为米色脂肪组织（“白色脂肪组织棕色”），从而改善了信号通路和整体肝功能。线粒体生物合成和功能的改善对于防止肝脂肪变性发展为NASH和肝硬化以及预防心血管并发症至关重要。