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首页> 外文期刊>Autophagy >Insufficient autophagy: a novel autophagic flux scenario uncovered by impaired liver TFEB-mediated lysosomal biogenesis from chronic alcohol-drinking mice
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Insufficient autophagy: a novel autophagic flux scenario uncovered by impaired liver TFEB-mediated lysosomal biogenesis from chronic alcohol-drinking mice

机译：自噬不充分：肝脏TFEB介导的血糖饮用小鼠介导的肝脏溶酶体生物发生越来越多的自噬磁通情况

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摘要

Macroautophagy/autophagy is a dynamic process, and newly synthesized autophagosomes need to fuse with lysosomes to complete the full process, which is referred to as autophagic degradation or autophagic flux. Therefore, the proper number and function of lysosomes are critical for accomplishing autophagic flux. In a recent study, we found that chronic ethanol consumption impairs TFEB (transcription factor EB) function, which leads to decreased lysosomal biogenesis resulting in hepatic steatosis and liver injury in mice. Interestingly, using the autophagic flux assay recommended by the autophagy guidelines, we discovered a novel autophagic flux scenario, which we termed insufficient autophagy. Insufficient autophagy is a scenario in which cells have a decreased number of lysosomes resulting in the accumulation of early autophagosomes. Insufficient autophagy is marked by a partially increased autophagic flux, but the process cannot reach its full degradative capacity due to the lack of a sufficient number of lysosomes. Our work demonstrated that pharmacological or genetic activation of TFEB-mediated lysosomal biogenesis enhances autophagic flux coupled with mitochondrial biogenesis in protecting against ethanol-induced liver injury. Overall, these findings not only identified the steps in which chronic ethanol impairs autophagic flux, but also discovered insufficient autophagy as a novel previously unappreciated autophagic flux scenario.
机译：宏观摄影/自噬是一种动态过程，新合成的自噬体需要融合溶酶体以完成完整的过程，其被称为自噬降解或自噬助剂。因此，溶酶体的适当数量和功能对于实现自噬助焊剂至关重要。在最近的一项研究中，我们发现慢性乙醇消耗损害TFEB（转录因子EB）功能，这导致溶酶体生物发生降低，导致小鼠的肝脏脂肪变性和肝损伤。有趣的是，使用自噬指南建议的自噬助噬核算，我们发现了一种新型的自噬磁通情景，我们称之为自噬不足。自噬不充分是一种情况，其中细胞具有降低的溶酶体数量，导致早期自噬体的积累。由于部分增加的自噬助焊剂标记了不充分的自噬，但由于缺乏足够数量的溶酶体，该过程不能达到其完全降解的能力。我们的作品表明，TFEB介导的溶酶体生物发生的药理或遗传活化增强了与线粒体生物发生的自噬通量，用于保护乙醇诱导的肝损伤。总体而言，这些发现不仅鉴定了慢性乙醇损害自噬助流的步骤，而且还发现了作为一种新的先前未被覆富的自噬助磁磁通情景的自噬不充分。

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