Cumulating evidence suggest that Zn2+ dys/homeostasis can play a major role in promoting brain injury in excitotoxic syndromes. Zn2+ homeostasis in the brain is regulated through highly dynamic pathways and is deeply connected with other major signaling pathways, such as NO- and MAP kinase-dependent systems. Zn2+ signaling in neurons and glia also interplays with proton and Ca2+ homeostasis. Zn2+ appears to promote injury with greater potency compared to Ca2+ and as such the cation may be an underappreciated mediator of excitotoxicity, which for many years has been described mainly as a Ca2+- dependent phenomenon. © 2007 Springer-Verlag US.

Zinc homeostasis and brain injury

Sensi S.
Primo
;
2007-01-01

Abstract

Cumulating evidence suggest that Zn2+ dys/homeostasis can play a major role in promoting brain injury in excitotoxic syndromes. Zn2+ homeostasis in the brain is regulated through highly dynamic pathways and is deeply connected with other major signaling pathways, such as NO- and MAP kinase-dependent systems. Zn2+ signaling in neurons and glia also interplays with proton and Ca2+ homeostasis. Zn2+ appears to promote injury with greater potency compared to Ca2+ and as such the cation may be an underappreciated mediator of excitotoxicity, which for many years has been described mainly as a Ca2+- dependent phenomenon. © 2007 Springer-Verlag US.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11564/824116
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