Recycling the danger via lipid droplet biogenesis after autophagy
Recycling the danger via lipid droplet biogenesis after autophagy
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DOI：
10.1080/15548627.2017.1371394
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发表时间：
2017-01-01
期刊：
影响因子：
13.3
通讯作者：
Ding, Wen-Xing
中科院分区：
文献类型：
--
作者：
Li, Yuan;Zong, Wei-Xing;Ding, Wen-Xing
脂肪酸是饥饿条件下重要的细胞能量来源。然而，细胞质中过多的游离脂肪酸（FFAs）会引起脂肪毒性。因此，了解细胞动员脂质和维持脂肪酸稳态水平的机制是很重要的。最近的证据表明，在饥饿条件下，细胞可以通过PNPLA2/脂肪甘油三酯脂肪酶和一种选择性的巨噬/自噬（称为脂噬）来分解脂滴（LDs），即储存中性脂质的胞内细胞器，以释放游离脂肪酸。由LD分解代谢产生的游离脂肪酸要么被运送到线粒体进行β氧化，要么被转化回LD。饥饿条件下LDs的生物发生是通过膜细胞器的自噬降解介导的，需要二酰基甘油o -酰基转移酶1，这是一种抗脂肪毒性的适应性细胞保护机制。
Fatty acids are an important cellular energy source under starvation conditions. However, excessive free fatty acids (FFAs) in the cytoplasm cause lipotoxicity. Therefore, it is important to understand the mechanisms by which cells mobilize lipids and maintain a homeostatic level of fatty acids. Recent evidence suggests that cells can break down lipid droplets (LDs), the intracellular organelles that store neutral lipids, via PNPLA2/adipose triglyceride lipase and a selective type of macroautophagy/autophagy termed lipophagy, to release FFAs under starvation conditions. FFAs generated from LD catabolism are either transported to mitochondria for beta-oxidation or converted back to LDs. The biogenesis of LDs under starvation conditions is mediated by autophagic degradation of membranous organelles and requires diacylglycerol O-acyltransferase 1, which serves as an adaptive cellular protective mechanism against lipotoxicity.