Matches in SemOpenAlex for { <https://semopenalex.org/work/W2054360166> ?p ?o ?g. }
- W2054360166 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." @default.
- W2054360166 created "2016-06-24" @default.
- W2054360166 creator A5004638032 @default.
- W2054360166 creator A5012586038 @default.
- W2054360166 creator A5032539937 @default.
- W2054360166 creator A5043783755 @default.
- W2054360166 creator A5049728625 @default.
- W2054360166 date "2015-03-02" @default.
- W2054360166 modified "2023-10-12" @default.
- W2054360166 title "Non-NMDAR neuronal Ca2+–permeable channels in delayed neuronal death and as potential therapeutic targets for ischemic brain damage" @default.
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