Cell death mechanisms and modulation in traumatic brain injury.

Cell death mechanisms and modulation in traumatic brain injury.
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DOI:
10.1016/j.nurt.2009.10.023
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发表时间:
2010-01
期刊:
Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
影响因子:
--
通讯作者:
Faden AI
Faden AI
中科院分区:
其他
文献类型:
--
作者:
Stoica BA;Faden AI

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创伤性脑损伤(TBI)后的细胞死亡是神经功能缺损和死亡的主要原因。了解延迟性创伤后细胞丢失的机制可能会导致改善结果的新疗法。虽然TBI诱导多种细胞类型的变化,神经元细胞死亡的机制一直是主要的焦点。最近的工作强调了神经元死亡表型的多样性,通常通过形态学或分子变化来定义。这导致了混乱,有时甚至是相互矛盾的术语。在这里,我们回顾了历史的基础上提出的神经元细胞死亡的定义,澄清关键的研究问题和治疗TBI的影响的目标。我们认为,形态学和分子特征必须用于澄清创伤后细胞死亡和相关的治疗目标。此外,我们强调,最有效的神经保护策略将需要针对多个途径,并反映不同的神经元细胞死亡表型的区域和时间的变化。
Cell death following traumatic brain injury (TBI) is a major cause of neurological deficits and mortality. Understanding mechanisms of delayed post-traumatic cell loss may lead to new therapies that improve outcome. Although TBI induces changes in multiple cell types, mechanisms of neuronal cell death have been the predominant focus. Recent work has emphasized the diversity of neuronal death phenotypes, which have generally been defined by either morphological or molecular changes. This has lead to confusing and at times contradictory nomenclature. Here we review the historical basis of proposed definitions of neuronal cell death with the goal of clarifying critical research questions and implications for therapy in TBI. We believe that both morphological and molecular features must be used to clarify post-traumatic cell death and related therapeutic targets. Further, we underscore that the most effective neuroprotective strategies will need to target multiple pathways and reflect the regional and temporal changes underlying diverse neuronal cell death phenotypes.
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