Oxidative stress, DNA damage, and the telomeric complex as therapeutic targets in acute neurodegeneration.
Oxidative stress, DNA damage, and the telomeric complex as therapeutic targets in acute neurodegeneration.
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DOI：
10.1016/j.neuint.2013.02.013
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发表时间：
2013-04
影响因子：
4.2
通讯作者：
Banik NL
中科院分区：
文献类型：
--
作者：
Smith JA;Park S;Krause JS;Banik NL
氧化应激已被确定为与急性CNS损伤和疾病如脊髓损伤（SCI）、创伤性脑损伤（TBI）和缺血性中风相关的神经变性的重要促成因素。在这篇综述中，我们简要地详细介绍了氧化应激（脂质过氧化，蛋白质氧化等）的损伤作用。特别强调DNA损伤。沿着其对神经元活力的下游效应，提出了急性CNS损伤中DNA损伤的证据。特别是，未经检查的氧化性DNA损伤引发一系列信号传导事件（例如p53和PARP-1的激活，细胞周期再激活），这些事件已显示促进CNS损伤后的神经元损失。这些发现表明，防止DNA损伤可能是促进神经元存活和增强这些条件下神经恢复的有效方法。最后，我们确定了端粒和端粒相关蛋白（如端粒酶）作为新的治疗靶点，在神经退行性疾病的治疗，由于其调节神经元对氧化应激和DNA损伤的反应的能力。
Oxidative stress has been identified as an important contributor to neurodegeneration associated with acute CNS injuries and diseases such as spinal cord injury (SCI), traumatic brain injury (TBI), and ischemic stroke. In this review, we briefly detail the damaging effects of oxidative stress (lipid peroxidation, protein oxidation, etc.) with a particular emphasis on DNA damage. Evidence for DNA damage in acute CNS injuries is presented along with its downstream effects on neuronal viability. In particular, unchecked oxidative DNA damage initiates a series of signaling events (e.g. activation of p53 and PARP-1, cell cycle re-activation) which have been shown to promote neuronal loss following CNS injury. These findings suggest that preventing DNA damage might be an effective way to promote neuronal survival and enhance neurological recovery in these conditions. Finally, we identify the telomere and telomere-associated proteins (e.g. telomerase) as novel therapeutic targets in the treatment of neurodegeneration due to their ability to modulate the neuronal response to both oxidative stress and DNA damage.
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影响因子：
4
作者：
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通讯作者：
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影响因子：
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DOI：
10.1073/pnas.1204156109
发表时间：
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影响因子：
11.1
作者：
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通讯作者：
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影响因子：
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