Disruption of Plin5 degradation by CMA causes lipid homeostasis imbalance in NAFLD
Disruption of Plin5 degradation by CMA causes lipid homeostasis imbalance in NAFLD
复制标题
CMA 破坏 Plin5 降解导致 NAFLD 中脂质稳态失衡
DOI：
10.1111/liv.14492
复制
发表时间：
2020-06-07
影响因子：
6.7
通讯作者：
Han, Ying
中科院分区：
文献类型：
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作者：
Ma, Shuo Y.;Sun, Ke S.;Han, Ying
非酒精性脂肪性肝病（NAFLD）的病理标志是肝脏脂质稳态失衡，其中脂肪吞噬作用已被发现起着至关重要的作用。然而，潜在的分子机制仍不清楚。我们研究了分子伴侣介导的自噬（CMA）在NAFLD发病机制中的作用。
The pathological hallmark of nonalcoholic fatty liver disease (NAFLD) is an imbalance in hepatic lipid homeostasis, in which lipophagy has been found to play a vital role. However, the underlying molecular mechanisms remain unclear. We investigated the role of chaperone‐mediated autophagy (CMA) in the pathogenesis of NAFLD.