Autophagy is a conserved quality-control pathway that degrades cytoplasmic contents in lysosomes. Autophagy degrades lipid droplets through a process termed lipophagy. Starvation and an acute lipid stimulus increase autophagic sequestration of lipid droplets and their degradation in lysosomes. Accordingly, liver-specific deletion of the autophagy gene Atg7 increases hepatic fat content, mimicking the human condition termed nonalcoholic fatty liver disease. In this review, we provide insights into the molecular regulation of lipophagy, discuss fundamental questions related to the mechanisms by which autophagosomes recognize lipid droplets and how ATG proteins regulate membrane curvature for lipid droplet sequestration, and comment on the possibility of cross talk between lipophagy and cytosolic lipases in lipid mobilization. Finally, we discuss the contribution of lipophagy to the pathophysiology of human fatty liver disease. Understanding how lipophagy clears hepatocellular lipid droplets could provide new ways to prevent fatty liver disease, a major epidemic in developed nations.

中文翻译：

---

肝脏中的自噬和脂质滴。

自噬是一种保守的质量控制途径，可降解溶酶体中的细胞质含量。自噬通过称为脂质吞噬的过程降解脂质小滴。饥饿和急性脂质刺激会增加脂质滴的自噬隔离，并在溶酶体中降解。因此，自噬基因Atg7的肝脏特异性缺失增加了肝脂肪含量，模仿了称为非酒精性脂肪肝疾病的人类疾病。在这篇综述中，我们提供了对脂质吞噬的分子调控的见解，讨论了与自噬小体识别脂质滴的机理以及ATG蛋白如何调节膜曲率以隔离脂质滴的机制相关的基本问题，并评论了脂质吞噬和脂质吞噬之间的相互影响的可能性。脂质动员中的胞质脂肪酶。最后，我们讨论了脂肪吞噬对人类脂肪肝疾病病理生理的贡献。了解脂吞噬作用如何清除肝细胞脂质滴可能提供预防脂肪肝疾病的新方法，脂肪肝疾病是发达国家的主要流行病。