Abstract:
:Endoplasmic reticulum (ER) stress induces a variety of neuronal cell death pathways that play a critical role in the pathophysiology of stroke. ER stress occurs when unfolded/misfolded proteins accumulate and the folding capacity of ER chaperones exceeds the capacity of ER lumen to facilitate their disposal. As a consequence, a complex set of signaling pathways will be induced that transmit from ER to cytosol and nucleus to compensate damage and to restore the normal cellular homeostasis, collectively known as unfolded protein response (UPR). However, failure of UPR due to severe or prolonged stress leads to cell death. Following acute CNS injuries, chronic disturbances in protein folding and oxidative stress prolong ER stress leading to sustained ER dysfunction and neuronal cell death. While ER stress responses have been well studied after stroke, there is an emerging need to study the association of ER stress with other cell pathways that exacerbate neuronal death after an injury. In this review, we summarize the current understanding of the role for ER stress in acute brain injuries, highlighting the diverse molecular mechanisms associated with ER stress and its relation to oxidative stress and autophagy. We also discussed the existing and developing therapeutic options aimed to reduce ER stress to protect the CNS after acute injuries.
journal_name
Mol Neurobioljournal_title
Molecular neurobiologyauthors
Nakka VP,Prakash-Babu P,Vemuganti Rdoi
10.1007/s12035-014-9029-6subject
Has Abstractpub_date
2016-01-01 00:00:00pages
532-544issue
1eissn
0893-7648issn
1559-1182pii
10.1007/s12035-014-9029-6journal_volume
53pub_type
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pub_type: 杂志文章
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pub_type: 杂志文章,评审
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