About this Research Topic
Despite intense research efforts over the last decades, the underlying cellular mechanisms that are involved in brain ischemia and neurodegenerative diseases are not fully understood. It is a complex interplay of different pathophysiological signal pathways which refer to oxidative stress, energy deprivation, inflammation and cell death. Herein, a stress signal cascade in the endoplasmic reticulum (ER), the so-called unfolded protein response (UPR) turned out to be a cellular hub which links neuronal degradation to a deregulated ER balance.
Although the UPR is regarded as a general survival mechanism in the short term and its prolonged activation seems to favor apoptosis, the cellular outcome cannot be predicted accurately and needs further investigation to clarify the role of each branch of the ER stress response.
This Research Topic welcomes Original Research and Review articles that help to improve understanding of the distinct ER stress responses and their contribution to neurological cell fate. Besides others, we would like to cover the following issues:
1) Which upstream regulators are involved in activation of the UPR pathways IRE1, ATF6 and PERK and can they be modulated for a beneficial outcome?
2) Are new small molecules available that target specific UPR targets and show low cellular toxicity?
3) Is there an equal activation pattern of the UPR branches in different neurodegenerative diseases and does it cause a similar cellular outcome?
4) How critical is the ER-associated degradation system (ERAD) for ER stress initiation and progression in neurodegenerative disorders?
5) What other cellular signaling pathways are influenced by ER stress?
Keywords: ER Homeostasis, ER Stress, UPR, Brain Ischemia, Neurodegeneration
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