Steatosis is an early characteristic in the pathogenesis of fatty liver disease (FLD). Mechanisms of hepatic steatosis are aetiology-dependent. Activation of autophagy in liver ameliorates hepatic steatosis. A modulation of hepatic autophagy affects the degree of hepatocyte steatosis and the progression of FLD as demonstrated by pre-clinical models and clinical trials. This review summarises recent advances on pathophysiological roles of autophagy in hepatic lipid metabolism. A comprehensive regulation of autophagic networks holds promise for the improvement of hepatic steatosis. Autophagic signalling pathway may be a novel therapeutic target against FLD.Highlights: •Hepatic steatosis is a pathological condition wherein vacuoles of triglyceride (TG) fat are overaccumulated in liver because of abnormal metabolism of lipids.•Hepatic autophagy regulates lipid metabolism as demonstrated by macrolipophagy in response to starvation and hepatic overabundance of TG in obesity.•Autophagic signals are closely associated with apoptotic pathways. There is distinctive relationship between hepatic autophagy and apoptosis, which affects the progression of fatty liver.•Regulation of autophagic process can be a novel therapeutic strategy for fatty liver disease.

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肝脂肪变性的分子机制：自噬的病理生理作用

脂肪变性是脂肪肝疾病 (FLD) 发病机制的早期特征。肝脂肪变性的机制依赖于病因。肝脏中自噬的激活可改善肝脏脂肪变性。正如临床前模型和临床试验所证明的，肝脏自噬的调节会影响肝细胞脂肪变性的程度和 FLD 的进展。本综述总结了自噬在肝脏脂质代谢中的病理生理作用的最新进展。自噬网络的全面调控有望改善肝脂肪变性。自噬信号通路可能是针对 FLD 的新型治疗靶点。亮点：•肝性脂肪变性是由于脂质代谢异常，甘油三酯（TG）脂肪液泡在肝脏中过度积累的一种病理状态。•肝脏自噬调节脂质代谢，如巨脂噬所证明的那样，对肥胖症患者的饥饿和肝脏过多的 TG 作出反应。•自噬信号与凋亡途径密切相关。肝脏自噬与细胞凋亡之间存在明显的关系，从而影响脂肪肝的进展。•自噬过程的调节可能是脂肪肝疾病的一种新的治疗策略。