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Endoplasmic reticulum stress in beta cells and autoimmune diabetes.
Current Opinion in Immunology ( IF 6.6 ) Pub Date : 2016-10-09 , DOI: 10.1016/j.coi.2016.09.006
Amy L Clark 1 , Fumihiko Urano 2
Affiliation  

Type 1 diabetes results from the autoimmune destruction of pancreatic β cells, leading to insulin deficiency and hyperglycemia. Although multiple attempts have been made to slow the autoimmune process using immunosuppressive or immunomodulatory agents, there are still no effective treatments that can delay or reverse the progression of type 1 diabetes in humans. Recent studies support endoplasmic reticulum (ER) as a novel target for preventing the initiation of the autoimmune reaction, propagation of inflammation, and β cell death in type 1 diabetes. This review highlights recent findings on ER stress in β cells and development of type 1 diabetes and introduces potential new treatments targeting the ER to combat this disorder.

中文翻译:

β细胞中的内质网应激和自身免疫性糖尿病。

1型糖尿病是由胰腺β细胞的自身免疫性破坏引起的,导致胰岛素缺乏和高血糖。尽管已经多次尝试使用免疫抑制剂或免疫调节剂来减缓自身免疫过程,但仍然没有有效的治疗方法可以延缓或逆转人类 1 型糖尿病的进展。最近的研究支持内质网 (ER) 作为预防 1 型糖尿病中自身免疫反应启动、炎症传播和 β 细胞死亡的新靶点。这篇综述重点介绍了 β 细胞 ER 应激和 1 型糖尿病发展的最新发现,并介绍了针对 ER 以对抗这种疾病的潜在新疗法。
更新日期:2016-10-05
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