Endoplasmic reticulum stress in hepatic steatosis and inflammatory bowel diseases.
Endoplasmic reticulum stress in hepatic steatosis and inflammatory bowel diseases.
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DOI：
10.3389/fgene.2014.00242
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发表时间：
2014
影响因子：
3.7
通讯作者：
Li Z
中科院分区：
文献类型：
--
作者：
Guo B;Li Z
内质网应激作为一种对内质网（endoplasmic reticulum，ER）中错误折叠蛋白超载的适应性反应，在维持分泌途径中蛋白质稳态以避免对宿主的损害方面起着关键作用。这种保守的机制是通过三个精心策划的途径来实现的，这些途径统称为未折叠蛋白反应（UPR）。持续的和病理性的ER应激与代谢、炎症和恶性疾病中的多种疾病有关。此外，ER应激通过UPR途径与炎症直接相关，UPR途径调节转录程序以诱导炎症基因的表达。重要的是，ER应激诱导的炎症反应是代谢性和炎症性疾病的发病机制的直接原因。在这篇综述中，我们将讨论连接ER应激与炎症的潜在信号通路。我们还将描述ER应激和炎症在肝脂肪变性、炎症性肠病和结肠炎相关结肠癌发病机制中的相互作用。
As an adaptive response to the overloading with misfolded proteins in the endoplasmic reticulum (ER), ER stress plays critical roles in maintaining protein homeostasis in the secretory pathway to avoid damage to the host. Such a conserved mechanism is accomplished through three well-orchestrated pathways known collectively as unfolded protein response (UPR). Persistent and pathological ER stress has been implicated in a variety of diseases in metabolic, inflammatory, and malignant conditions. Furthermore, ER stress is directly linked with inflammation through UPR pathways, which modulate transcriptional programs to induce the expression of inflammatory genes. Importantly, the inflammation induced by ER stress is directly responsible for the pathogenesis of metabolic and inflammatory diseases. In this review, we will discuss the potential signaling pathways connecting ER stress with inflammation. We will also depict the interplay between ER stress and inflammation in the pathogenesis of hepatic steatosis, inflammatory bowel diseases and colitis-associated colon cancer.
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影响因子：
5.2
作者：
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通讯作者：
Chan SW
影响因子：
29.7
作者：
Davis BK;Wen H;Ting JP
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影响因子：
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DOI：
10.1074/jbc.m111.228817
发表时间：
2011-10-21
期刊：
The Journal of biological chemistry
影响因子：
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通讯作者：
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影响因子：
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作者：
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