Regen Med Res
Volume 2, 2014
|Number of page(s)||6|
|Published online||23 July 2014|
Promising targets of cell death signaling of NR2B receptor subunit in stroke pathogenesis
Department of Pathophysiology, Tongji Medical College and Institute for Brain Research, Huazhong University of Science and Technology, 13# Hangkong Road, Wuhan 430030, PR China
* Correspondence: firstname.lastname@example.org
Received: 15 March 2014
Accepted: 10 July 2014
Stroke is an acute cerebrovascular disease caused by acute brain artery bursting or cerebral embolism that leads to neuronal death and severe dysfunction of synaptic transmission. Neuronal damage after stroke remains a major cause of morbidity and mortality worldwide and affects 795 000 of lives every year in United States. However, effective treatments remain lacking, which makes the identification of new therapeutic targets a matter of great importance.
N-methyl-D-aspartate glutamate (NMDA) receptor is important both in the normal synaptic transmission and in the neuronal death after stroke. Accumulated evidences show NMDA receptor downstream effectors, such as PSD-95, DAPK1, and ERK, had been revealed to be linked with neuronal damage. Based on our recent studies, we review the promising targets of the NMDA receptor downstream signaling involved in stroke treatment. This review will provide the concept of NR2B downstream signaling in neuronal death after stroke and provide evidences for developing better NMDAR-based therapeutics by targeting downstream proteins.
Key words: Stroke / DAPK1 / NMDA receptor / Neuronal death
© 2014 Shu et al.; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
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