Loss of endoplasmic reticulum Ca2＋ homeostasis： contribution to neuronal cell death during cerebral ischemia

The loss of Ca2＋ homeostasis during cerebral ischemia is a hallmark of impending neuronal demise. Accordingly, considerable cellular resources are expended in maintaining low resting cytosolic levels of Ca2＋. These include contributions by a host of proteins involved in the sequestration and transpo...

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Bibliographic Details
Published in:Acta pharmacologica Sinica 2013-01, Vol.34 (1), p.49-59
Main Authors: Bodalia, Ankur, Li, Hongbin, Jackson, Michael F
Format: Article
Language:English
Subjects:
Animals
Brain - blood supply
Brain - metabolism
Brain - pathology
Brain Ischemia - metabolism
Brain Ischemia - pathology
Calcium - metabolism
Cell Death
Endoplasmic Reticulum - metabolism
Endoplasmic Reticulum - pathology
Endoplasmic Reticulum Stress
Homeostasis
Humans
Neurons - metabolism
Neurons - pathology
Review
Unfolded Protein Response
信号转导通路
内质网
损失
死亡过程
神经元损伤
神经细胞
脑缺血
钙稳态
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Summary:The loss of Ca2＋ homeostasis during cerebral ischemia is a hallmark of impending neuronal demise. Accordingly, considerable cellular resources are expended in maintaining low resting cytosolic levels of Ca2＋. These include contributions by a host of proteins involved in the sequestration and transport of Ca2＋, many of which are expressed within intracellular organelles, including lysosomes, mitochon- dria as well as the endoplasmic reticulum （ER）. Ca2＋ sequestration by the ER contributes to cytosolic Ca2＋ dynamics and homeosta- sis. Furthermore, within the ER Ca2＋ plays a central role in regulating a host of physiological processes. Conversely, impaired ER Ca2＋ homeostasis is an important trigger of pathological processes. Here we review a growing body of evidence suggesting that ER dysfunc- tion is an important factor contributing to neuronal injury and loss post-ischemia. Specifically, the contribution of the ER to cytosolic Ca2＋ elevations during ischemia will be considered, as will the signalling cascades recruited as a consequence of disrupting ER home- ostasis and function.
ISSN:1671-4083
1745-7254
DOI:10.1038/aps.2012.139