Oxidative stress and DNA damage after cerebral ischemia: Potential therapeutic targets to repair the genome and improve stroke recovery.
Oxidative stress and DNA damage after cerebral ischemia: Potential therapeutic targets to repair the genome and improve stroke recovery.
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脑缺血后的氧化应激和 DNA 损伤：修复基因组和改善中风恢复的潜在治疗靶点
DOI：
10.1016/j.neuropharm.2017.11.011
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发表时间：
2018-05-15
影响因子：
4.7
通讯作者：
Chen J
中科院分区：
文献类型：
--
作者：
Li P;Stetler RA;Leak RK;Shi Y;Li Y;Yu W;Bennett MVL;Chen J
在过去的二十年里，氧化应激研究取得了显着进展，特别是在缺血性脑损伤的背景下。缺血组织中的氧化应激损害基因组的完整性，导致DNA损伤，神经元、神经胶质细胞和血管细胞的细胞死亡，以及中风后神经恢复的障碍。由于DNA特别容易受到氧化攻击，细胞已经进化出诱导多种DNA修复机制的能力，包括碱基切除修复（BER），核苷酸切除修复（NER）和非同质端点连接（NHEJ）。DNA修复缺陷与卒中后神经功能预后不良密切相关，而DNA修复酶如APE 1、OGG 1和XRCC 1的上调可改善卒中后的长期功能恢复。事实上，现在已知DNA损伤和修复在中风恢复的基本方面，如神经发生、白色物质恢复和神经血管单位重塑中起关键作用。几种DNA修复酶对卒中后的综合神经修复机制至关重要，包括用于神经发生的Polβ和NEIL 3，用于白色修复的APE 1，用于轴突再生的Gadd 45 b和用于神经血管重塑的DNA-PKs。本文综述了DNA损伤和修复在脑卒中后功能恢复中的作用，并强调了DNA修复对脑卒中后再生因素的贡献。
The past two decades have witnessed remarkable advances in oxidative stress research, particularly in the context of ischemic brain injury. Oxidative stress in ischemic tissues compromises the integrity of the genome, resulting in DNA lesions, cell death in neurons, glial cells, and vascular cells, and impairments in neurological recovery after stroke. As DNA is particularly vulnerable to oxidative attack, cells have evolved the ability to induce multiple DNA repair mechanisms, including base excision repair (BER), nucleotide excision repair (NER) and non-homogenous endpoint jointing (NHEJ). Defective DNA repair is tightly correlated with worse neurological outcomes after stroke, whereas upregulation of DNA repair enzymes, such as APE1, OGG1, and XRCC1, improves long-term functional recovery following stroke. Indeed, DNA damage and repair are now known to play critical roles in fundamental aspects of stroke recovery, such as neurogenesis, white matter recovery, and neurovascular unit remodeling. Several DNA repair enzymes are essential for comprehensive neural repair mechanisms after stroke, including Polβ and NEIL3 for neurogenesis, APE1 for white matter repair, Gadd45b for axonal regeneration, and DNA-PKs for neurovascular remodeling. This review discusses the emerging role of DNA damage and repair in functional recovery after stroke and highlights the contribution of DNA repair to regenerative elements after stroke.
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影响因子：
5.6
作者：
ElAli A;Thériault P;Rivest S
通讯作者：
Rivest S
DOI：
10.1038/jcbfm.2009.187
发表时间：
2010-01
期刊：
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
影响因子：
--
作者：
通讯作者：
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DNA-PKcs 在响应 DNA 损伤和细胞周期进展的 H2AX 磷酸化调节中起主导作用。
影响因子：
--
作者：
An J;Huang YC;Xu QZ;Zhou LJ;Shang ZF;Huang B;Wang Y;Liu XD;Wu DC;Zhou PK
通讯作者：
Zhou PK
通过增强血管生成和血管生成，粒细胞刺激性刺激因子减弱了缺血性卒中大鼠TPA诱导的出血转化。
DOI：
10.1038/jcbfm.2014.208
发表时间：
2015-02
期刊：
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
影响因子：
--
作者：
通讯作者：
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影响因子：
37.8
作者：
Benjamin, Emelia J.;Virani, Salim S.;Muntner, Paul
通讯作者：
Muntner, Paul