Chromatin-modifying agents for epigenetic reprogramming and endogenous neural stem cell-mediated repair in stroke.
Chromatin-modifying agents for epigenetic reprogramming and endogenous neural stem cell-mediated repair in stroke.
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DOI：
10.1007/s12975-010-0051-3
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发表时间：
2011-03-01
影响因子：
6.9
通讯作者：
Mehler MF
中科院分区：
文献类型：
--
作者：
Qureshi IA;Mehler MF
最近对表观遗传学和染色质生物学的兴趣激增，对我们对脑缺血病理生理学的理解产生了重大影响，并导致了中风新治疗策略的确定，例如采用组蛋白脱乙酰酶抑制剂的策略。这些都是关键的进步；然而，染色质生物学的快速发现和染色质修饰剂开发的创新意味着新兴的药物类别也可能对中风具有潜在益处。在这里，我们讨论了各种染色质调节因子及其最近发现的抑制剂如何分别作为中风的药物靶点和治疗剂。这些因子主要包括阻遏元件1沉默转录因子（REST）/神经元限制性沉默因子大分子复合物、多梳族（PcG）蛋白和相关染色质重塑因子的成员，这些因子与脑缺血的病理生理学有关。此外，我们认为，由于 REST、PcG 蛋白和其他染色质重塑因子在神经干和祖细胞 (NSPC) 生物学中发挥的关键作用，染色质修饰剂不仅可用于直接减轻缺血性损伤，而且还可能促进内源性 NSPC 介导的脑修复机制。
The recent explosion of interest in epigenetics and chromatin biology has made a significant impact on our understanding of the pathophysiology of cerebral ischemia and led to the identification of new treatment strategies for stroke, such as those that employ histone deacetylase inhibitors. These are key advances; however, the rapid pace of discovery in chromatin biology and innovation in the development of chromatin-modifying agents implies there are emerging classes of drugs that may also have potential benefits in stroke. Herein, we discuss how various chromatin regulatory factors and their recently identified inhibitors may serve as drug targets and therapeutic agents for stroke, respectively. These factors primarily include members of the repressor element-1 silencing transcription factor (REST)/neuron-restrictive silencer factor macromolecular complex, polycomb group (PcG) proteins, and associated chromatin remodeling factors, which have been linked to the pathophysiology of cerebral ischemia. Further, we suggest that, because of the key roles played by REST, PcG proteins and other chromatin remodeling factors in neural stem and progenitor cell (NSPC) biology, chromatin-modifying agents can be utilized not only to mitigate ischemic injury directly but also potentially to promote endogenous NSPC-mediated brain repair mechanisms.
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影响因子：
11.2
作者：
Chen, Haobin;Yan, Yan;Costa, Max
通讯作者：
Costa, Max
DOI：
10.1073/pnas.96.17.9873
发表时间：
1999-08-17
影响因子：
11.1
作者：
Andrés, ME;Burger, C;Mandel, G
通讯作者：
Mandel, G
小分子和组蛋白底物类似物作为LSD1赖氨酸脱甲基酶抑制剂的比较分析。
影响因子：
15
作者：
Culhane, Jeffrey C.;Wang, Dongqing;Yen, Paul M.;Cole, Philip A.
通讯作者：
Cole, Philip A.
缺血性脑损伤的干细胞：批判性综述。
DOI：
10.1002/cne.22038
发表时间：
2009-07-01
期刊：
The Journal of comparative neurology
影响因子：
--
作者：
Burns TC;Verfaillie CM;Low WC
通讯作者：
Low WC
影响因子：
4.5
作者：
Dekanty A;Romero NM;Bertolin AP;Thomas MG;Leishman CC;Perez-Perri JI;Boccaccio GL;Wappner P
通讯作者：
Wappner P