换一批
换一批内质网应激与2型糖尿病发病机制的关系
Relationship between endoplasmic reticulum stress and the pathogenesis of type 2 diabetes
摘要多种因素可以打破内质网的稳态,导致蛋白质折叠障碍或错误折叠,进而触发内质网应激(ERS).适度的ERS起适应性的细胞保护作用,而过高和持久的ERS则会激活特有的凋亡通路导致细胞凋亡.ERS通过影响胰岛细胞的功能、促使胰岛β细胞凋亡及参与胰岛素抵抗介导2型糖尿病的发生、发展.
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abstractsThe endoplasmic reticulum(ER) is exquisitely sensitive to alterations in homeostasis,and proteins formed in the ER may fail to attain correct conformation due to many factors. Accumulation of misfolded proteins that aggregate in the ER lumen causes ER stress(ERS). Morderate ERS contributes to adaptive cytoprotection, while excessive and prolonged ERS triggers cell apoptosis through activating unique apoptosis pathway. ERS plays a role in the pathogenesis of type 2 diabetes by affecting the function of islet beta cells, enhancing apoptosis in islet beta cells and insulin resistance.
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关键词
内质网应激细胞凋亡胰岛素抵抗2型糖尿病Endoplasmic reticulum stressApoptosisInsulin resistanceType 2 diabetes mellitus
主题词
内质网应激(Endoplasmic Reticulum Stress)糖尿病, 2型(Diabetes Mellitus, Type 2)细胞凋亡(Apoptosis)胰岛(Islets of Langerhans)内质网(Endoplasmic Reticulum)
分类号
R5
栏目名称
DOI
10.3760/cma.j.issn.1673-4157.2011.02.016
发布时间
2011-06-08
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