Journal
TRENDS IN PHARMACOLOGICAL SCIENCES
Volume 32, Issue 8, Pages 480-486Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tips.2011.04.001
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Funding
- NIGMS NIH HHS [P20 GM109089] Funding Source: Medline
- NINDS NIH HHS [R01 NS065219, R01 NS065219-01A1, R01 NS051288] Funding Source: Medline
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Cerebral ischemia is a leading cause of morbidity and mortality, reflecting the extraordinary sensitivity of the brain to a brief loss of blood flow. A significant goal has been to identify pathways of neuronal injury that are selectively activated after stroke and may be amenable to drug therapy. An important advance was made nearly 25 years ago when Ca2+ overload was implicated as a critical link between glutamate excitotoxicity and ischemic neurodegeneration. However, early hope for effective therapies faded as glutamate-targeted trials repeatedly failed to demonstrate efficacy in humans. In a review in 2000 in this journal, we described new evidence linking a related cation, zinc (Zn2+), to neuronal injury, emphasizing sources and mechanisms of Zn2+ toxicity. The current review highlights progress over the last decade, emphasizing mechanisms through which Zn2+ ions (from multiple sources) participate together with Ca2+ in different stages of cascades of ischemic injury.
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