Calpains and Delayed Calcium Deregulation in Excitotoxicity
Calpains and Delayed Calcium Deregulation in Excitotoxicity
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DOI：
10.1007/s11064-010-0323-z
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发表时间：
2010-12-01
影响因子：
4.4
通讯作者：
Carvalho, Arselio P.
中科院分区：
文献类型：
--
作者：
Araujo, Ines M.;Carreira, Bruno P.;Carvalho, Arselio P.
谷氨酸受体的过度激活会导致多种脑部病变，包括脑缺血、癫痫、创伤性脑损伤和进展缓慢的神经退行性疾病。在所有这些病理过程中，钙依赖的半胱氨酸蛋白酶、钙调蛋白是神经细胞死亡机制中的关键角色。许多研究小组一直在积极寻求建立与兴奋性毒性相关的细胞内钙稳态的解除调节与钙蛋白酶活性之间的联系。众所周知，这两个事件是相互联系和协同作用，促进神经退行性变，但钙蛋白酶的活性是否依赖于或促进了钙离子的解除调节仍存在争议。
Overactivation of glutamate receptors results in neurodegeneration in a variety of brain pathologies, including ischemia, epilepsy, traumatic brain injury and slow-progressing neurodegenerative disorders. In all these pathologies, it is well accepted that the calcium-dependent cysteine proteases calpains are key players in the mechanisms of neuronal cell death. Many research groups have been actively pursuing to establish a link between the deregulation of intracellular Ca2+ homeostasis associated with excitotoxicity and calpain activity. It is well established that these two events are connected and interact synergistically to promote neurodegeneration, but whether calpain activity depends on or contributes to Ca2+ deregulation is still under debate.