参与谷氨酸受体非依赖性缺血性脑损伤的钙通透性离子通道。
Calcium-permeable ion channels involved in glutamate receptor-independent ischemic brain injury.
机构信息
Department of Psychology, Washington State University, Vancouver, WA, USA.
出版信息
Acta Pharmacol Sin. 2011 Jun;32(6):734-40. doi: 10.1038/aps.2011.47. Epub 2011 May 9.
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.
摘要
脑缺血是全球范围内导致死亡和长期残疾的主要原因。不幸的是，目前的治疗方法仅限于溶栓，但其成功率有限，且存在潜在的脑出血副作用。寻找新的细胞损伤机制和治疗干预措施已成为该领域的主要挑战。多年来，人们已经认识到神经元内 Ca(2+)超载对于与脑缺血相关的神经元损伤至关重要。然而，导致有毒性 Ca(2+)负载的确切途径仍不清楚。本综述讨论了两种 Ca(2+)渗透性阳离子通道（TRPM7 和酸感应通道）在与脑缺血相关的谷氨酸非依赖性 Ca(2+)毒性中的作用。
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