Dysfunction of neuronal calcium signalling in neuroinflammation and neurodegeneration

被引:44
作者
Fairless, Richard [1 ]
Williams, Sarah K. [1 ]
Diem, Ricarda [1 ]
机构
[1] Univ Clin Heidelberg, Dept Neurooncol, D-69120 Heidelberg, Germany
关键词
Calcium signalling; Neuroinflammation; Neurodegeneration; Neurons; Autoimmunity; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; PRECLINICAL RETINAL NEURODEGENERATION; REGULATORY T-CELLS; MULTIPLE-SCLEROSIS; AXONAL-INJURY; SPINAL-CORD; SODIUM-CHANNELS; ANOXIC INJURY; CALPAIN ACTIVATION; OPTIC NEURITIS;
D O I
10.1007/s00441-013-1758-8
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Neurodegeneration has been increasingly recognised as the leading structural correlate of disability progression in autoimmune diseases such as multiple sclerosis. Since calcium signalling is known to regulate the development of degenerative processes in many cell types, it is believed to play significant roles in mediating neurodegeneration. Because of its function as a major juncture linking various insults and injuries associated with inflammatory attack on neuronal cell bodies and axons, it provides potential for the development of neuroprotective strategies. This is of great significance because of the lack of neuroprotective agents presently available to supplement the current array of immunomodulatory treatments. In this review, we summarise the role that various calcium channels and pumps have been shown to play in the development of neurodegeneration under inflammatory autoimmune conditions. The identification of suitable targets might also provide insights into applications in non-inflammatory neurodegenerative diseases.
引用
收藏
页码:455 / 462
页数:8
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