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Abstract：
The process of autophagy is integral to cellular function. In this process, proteins, organelles, and metabolites are engulfed in a lipid vesicle and trafficked to a lysosome for degradation. Its central role in protein and organelle homeostasis has piqued interest for autophagy dysfunction as a driver of pathology for a number of diseases including cancer, muscular disorders, neurological disorders, and non-alcoholic fatty liver disease. For much of its history, the study of autophagy has centered around proteins, however, due to advances in mass spectrometry and refined methodologies, the role of lipids in this essential cellular process has become more apparent. This review discusses the diverse endogenous lipid compounds shown to mediate autophagy. Downstream lipid signaling pathways are also reviewed in the context of autophagy regulation. Specific focus is placed upon the Mammalian Target of Rapamycin (mTOR) and Peroxisome Proliferator-Activated Receptor (PPAR) signaling pathways as integration hubs for lipid regulation of autophagy.
摘要：
自噬是细胞功能不可或缺的过程。在这个过程中,蛋白质，细胞器,和代谢物被吞噬在脂质囊泡中，并被运输到溶酶体进行降解。它在蛋白质和细胞器稳态中的中心作用引起了人们对自噬功能障碍的兴趣，作为包括癌症在内的许多疾病的病理驱动因素，肌肉疾病,神经系统疾病,和非酒精性脂肪性肝病。在它的大部分历史中，自噬的研究集中在蛋白质，然而,由于质谱和改进方法的进步，脂质在这个重要的细胞过程中的作用已经变得更加明显。这篇综述讨论了介导自噬的各种内源性脂质化合物。下游脂质信号通路也在自噬调节的背景下进行了综述。特别关注哺乳动物雷帕霉素靶标（mTOR）和过氧化物酶体增殖物激活受体（PPAR）信号通路，作为自噬脂质调节的整合枢纽。
