Endoplasmic reticulum stress and lipid metabolism: mechanisms and therapeutic potential.
Endoplasmic reticulum stress and lipid metabolism: mechanisms and therapeutic potential.
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DOI：
10.1155/2012/841362
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发表时间：
2012
影响因子：
3
通讯作者：
Austin RC
中科院分区：
文献类型：
--
作者：
Basseri S;Austin RC
内质网在蛋白质的折叠、组装和分泌中起着至关重要的作用。ER稳态的破坏可能导致错误折叠或未折叠蛋白质在ER腔中的积累，这种情况称为ER应激。响应于ER应激，被称为未折叠蛋白反应（UPR）的信号转导途径被激活。UPR激活允许细胞科普ER上增加的蛋白质折叠需求。最近的研究表明，ER应激/UPR激活在脂质代谢和稳态中起着关键作用。ER应激依赖性脂质代谢失调可能导致血脂异常、胰岛素抵抗、心血管疾病、2型糖尿病和肥胖。在本文中，我们研究了最近的研究结果，说明ER应激/UPR信号通路在调节脂质代谢中发挥的重要作用，以及它们如何导致脂质稳态失调。
The endoplasmic reticulum (ER) plays a crucial role in protein folding, assembly, and secretion. Disruption of ER homeostasis may lead to accumulation of misfolded or unfolded proteins in the ER lumen, a condition referred to as ER stress. In response to ER stress, a signal transduction pathway known as the unfolded protein response (UPR) is activated. UPR activation allows the cell to cope with an increased protein-folding demand on the ER. Recent studies have shown that ER stress/UPR activation plays a critical role in lipid metabolism and homeostasis. ER-stress-dependent dysregulation of lipid metabolism may lead to dyslipidemia, insulin resistance, cardiovascular disease, type 2 diabetes, and obesity. In this paper, we examine recent findings illustrating the important role ER stress/UPR signalling pathways play in regulation of lipid metabolism, and how they may lead to dysregulation of lipid homeostasis.