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- W2043133738 endingPage "740" @default.
- W2043133738 startingPage "734" @default.
- W2043133738 abstract "Brain ischemia is a leading cause of death and long-term disabilities worldwide. Unfortunately, current treatment is limited to thrombolysis, which has limited success and a potential side effect of intracerebral hemorrhage. Searching for new cell injury mechanisms and therapeutic interventions has become a major challenge in the field. It has been recognized for many years that intracellular Ca(2+) overload in neurons is essential for neuronal injury associated with brain ischemia. However, the exact pathway(s) underlying the toxic Ca(2+) loading remained elusive. This review discusses the role of two Ca(2+)-permeable cation channels, TRPM7 and acid-sensing channels, in glutamate-independent Ca(2+) toxicity associated with brain ischemia." @default.
- W2043133738 created "2016-06-24" @default.
- W2043133738 creator A5024433736 @default.
- W2043133738 creator A5034777038 @default.
- W2043133738 creator A5039568707 @default.
- W2043133738 creator A5085043923 @default.
- W2043133738 date "2011-05-09" @default.
- W2043133738 modified "2023-10-15" @default.
- W2043133738 title "Calcium-permeable ion channels involved in glutamate receptor-independent ischemic brain injury" @default.
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