Non-NMDAR neuronal Ca(2+)-permeable channels in delayed neuronal death and as potential therapeutic targets for ischemic brain damage

Expert Opinion on Therapeutic Targets
Chaokun LiLin-Hua Jiang

Abstract

Transient cerebral ischemia represents the most common cause of complex chronic disability in adults due to delayed neuronal death as a result of aberrant post-ischemic increases in the [Ca(2+)]c and [Zn(2+)]c. A number of Ca(2+)-permeable channels are engaged in transient ischemia-induced neuronal death. In this review, the authors discuss the GluA2-lacking AMPARs, acid-sensing ion channel 1a, melastatin-related transient receptor potential 2 (TRPM2), TRPM7 and store-operated Ca(2+) channels expressed in ischemia-vulnerable neurons, and focus on the studies using in vitro and in vivo models of transient ischemia that supports a significant role for these channels in inducing increases in the [Ca(2+)]c and/or [Zn(2+)]c and delayed neuronal death, and their potential as therapeutic targets. Non-NMDAR Ca(2+)-permeable channels are important mechanisms mediating delayed neuronal death and cognitive dysfunctions after transient ischemia. Identification of such Ca(2+)-permeable channels significantly improves our understanding of the molecular events leading to ischemic brain damage and provides promising novel targets for post-ischemic therapeutics treating ischemic brain damage.

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Citations

Aug 25, 2015·Frontiers in Immunology·Sharifah Alawieyah Syed MortadzaLin-Hua Jiang
Feb 16, 2017·Journal of Neuroscience Research·Frederik Boe HansenAsger Granfeldt
Mar 16, 2017·Antioxidants & Redox Signaling·Quan JiangFeng Han
Feb 7, 2020·International Journal of Molecular Sciences·Violetta O IvanovaNatalia V Bal
Nov 17, 2020·Frontiers in Neuroscience·Dennis W Choi

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