研究动态
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NFE2L1 在代谢和相关疾病中的多方面功能。

The multifaceted functions of NFE2L1 in metabolism and associated disorders.

发表日期:2024 Jul 09
作者: Xuye Zhao, Chang Xu, Yi Ding, Nianlong Yan
来源: LIFE SCIENCES

摘要:

核因子红细胞 2 相关因子 1(NFE2L1,也称为 Nrf1)是转录因子 CNC-bZIP 亚家族的重要成员,在我们体内普遍表达。最近的研究结果揭示了它与各种代谢过程的关联,包括葡萄糖、脂质和蛋白质代谢。在葡萄糖代谢领域,NFE2L1 通过调节胰腺 β 细胞和胰岛素的产生来发挥调节控制作用。它还影响肝脏的葡萄糖代谢和脂肪组织的胰岛素敏感性。关于脂质代谢,NFE2L1 通过影响肝脏和脂肪组织中特定的脂肪形成和脂肪分解基因的表达来控制这一过程。此外,NFE2L1 还调节特定的脂质,例如胆固醇。这些参与是 NFE2L1 缺陷的各种表现的基础,例如脂肪细胞肥大、炎症和脂肪性肝炎。在蛋白质代谢领域,NFE2L1 作为调节 26S 蛋白酶体基因表达的主要转录因子,其功能障碍与神经退行性疾病、癌症、自身免疫性疾病等多种疾病有关。在这篇综合综述中,我们总结了其不同的作用NFE2L1 在葡萄糖、脂质和蛋白质代谢中发挥作用,及其对与这些代谢过程相关的疾病的影响。版权所有 © 2024。由 Elsevier Inc. 出版。
Nuclear factor erythroid 2-related factor 1 (NFE2L1, also known as Nrf1) is a crucial member of the CNC-bZIP subfamily of transcription factors expressed ubiquitously throughout our body. Recent findings have revealed its association with various metabolic processes, encompassing glucose, lipid, and protein metabolism. In the realm of glucose metabolism, NFE2L1 exerts regulatory control by modulating pancreatic β cells and insulin production. It also influences glucose metabolism in liver and the insulin sensitivity of adipose tissue. Regarding lipid metabolism, NFE2L1 governs this process by influencing the expression of specific adipogenic and lipolysis genes in both liver and adipose tissue. Additionally, NFE2L1 regulates specific lipids, such as cholesterol. These involvements underlie various manifestations of NFE2L1 deficiency such as adipocyte hypertrophy, inflammation, and steatohepatitis. In the realm of protein metabolism, NFE2L1 serves as a major transcription factor regulating the 26S proteasome genes expression, which dysfunction has been related with multiple diseases including neurodegenerative diseases, cancers, autoimmune conditions, etc. In this comprehensive review, we summarize the diverse roles that NFE2L1 plays in glucose, lipid, and protein metabolism, as well as its impact on diseases related to these metabolic processes.Copyright © 2024. Published by Elsevier Inc.