期刊
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
卷 7, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2019.00084
关键词
endoplasm reticulum stress; aging; neurodegeneration; unfolded protein response; proteostasis
资金
- Canadian Institutes for Health Research [MOP-137041]
- Ontario Graduate Scholarship
Multiple factors lead to proteostatic perturbations, often resulting in the aberrant accumulation of toxic misfolded proteins. Cells, from yeast to humans, can respond to sudden accumulation of secretory proteins within the endoplasmic reticulum (ER) through pathways such as the Unfolded Protein Response (UPR). The ability of cells to adapt the ER folding environment to the misfolded protein burden ultimately dictates cell fate. The aging process is a particularly important modifier of the proteostasis network; as cells age, both their ability to maintain this balance in protein folding/degradation and their ability to respond to insults in these pathways can break down, a common element of age-related diseases (including neurodegenerative diseases). ER stress coping mechanisms are central to lifespan regulation under both normal and disease states. In this review, we give a brief overview of the role of ER stress response pathways in age-dependent neurodegeneration.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据