Calcium-permeable ion channels involved in glutamate receptor-independent ischemic brain injury

Ming Hua Li, Koichi Inoue, Hong Fang Si, Zhi Gang Xiong

Research output: Contribution to journalArticle

19 Scopus citations

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 Ca2+ overload in neurons is essential for neuronal injury associated with brain ischemia. However, the exact pathway(s) underlying the toxic Ca2+ loading remained elusive. This review discusses the role of two Ca2+-permeable cation channels, TRPM7 and acid-sensing channels, in glutamate-independent Ca2+ toxicity associated with brain ischemia.

Original languageEnglish (US)
Pages (from-to)734-740
Number of pages7
JournalActa Pharmacologica Sinica
Volume32
Issue number6
DOIs
StatePublished - Jun 1 2011

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Keywords

  • TRPM7
  • acid-sensing ion channel
  • brain ischemia
  • neurons

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)

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