Advances in secondary spinal cord injury - Role of apoptosis
Advances in secondary spinal cord injury - Role of apoptosis
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DOI：
10.1097/00007632-200007150-00022
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发表时间：
2000-07-15
期刊：
影响因子：
3
通讯作者：
Waite, P
中科院分区：
文献类型：
--
作者：
Lu, JK;Ashwell, KWS;Waite, P
脊髓损伤的结果取决于由原发损伤引起的一系列细胞和分子事件所产生的继发性损伤的程度。本文综述了继发性脊髓损伤涉及神经元和神经胶质细胞的凋亡和坏死死亡的证据。还讨论了可能导致细胞死亡的主要因素，如谷氨酸能兴奋毒性、自由基损伤、细胞因子和炎症。减少继发性脊髓损伤的创新治疗策略的发展取决于对继发性损伤机制在分子和生化水平上的进一步了解。这种治疗干预可能包括使用抗凋亡药物、自由基清除剂和抗炎剂。这些药物可以靶向阻断细胞和分子损伤级联的关键反应，从而减少继发性组织损伤，最大限度地减少副作用，并改善功能恢复。
The outcome of spinal cord injury depends on the extent of secondary damage produced by a series of cellular and molecular events initiated by the primary trauma. This article reviews the evidence that secondary spinal cord injury involves the apoptotic as well as necrotic death of neurons and glial cells. Also discussed are the major factors that can contribute to cell death, such as glutamatergic excitotoxicity, free radical damage, cytokines, and inflammation. The development of innovative therapeutic strategies to reduce secondary spinal cord injury depends on an increased understanding of secondary injury mechanisms at the molecular and biochemical level. Such therapeutic interventions may include the use bf antiapoptotic drugs, free radical scavengers, and antiinflammatory agents. These could be targeted to block key reactions on cellular and molecular injury cascades, thus reducing secondary tissue damage, minimizing side effects, and improving functional recovery.