Signaling pathways in reactive astrocytes, a genetic perspective.
Signaling pathways in reactive astrocytes, a genetic perspective.
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DOI：
10.1007/s12035-011-8163-7
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发表时间：
2011-06
影响因子：
5.1
通讯作者：
Hebert, Jean M.
中科院分区：
文献类型：
--
作者：
Kang, Wenfei;Hebert, Jean M.
反应性星形胶质细胞与大量中枢神经系统（CNS）病理学相关。星形胶质细胞的活化的特征在于其分子和形态特征的变化，并且取决于损伤的类型，还可以伴随炎症反应、神经元损伤，并且在严重的情况下，瘢痕形成。虽然反应性星形胶质细胞增生是抑制损伤所必需的正常生理反应，但它也可能对神经元存活和轴突再生产生有害影响，特别是在神经退行性疾病中。据信，星形胶质细胞在变得反应性时的进行性变化受到复杂的细胞间和细胞内信号传导机制的精细调节。然而，这些问题还有待解决。从体内和培养模式的功能获得方法中已经学到了很多，但在大多数情况下，缺乏功能丧失遗传学研究，这是一种重要的补充方法。了解哪些信号通路需要控制不同方面的星形胶质细胞增生将是必要的设计治疗策略，以提高其有益的影响，并限制其有害的CNS病理。在这篇文章中，我们回顾了最近的进展，在星形胶质细胞增生的调节方面的机制，主要集中在已使用功能丧失的遗传小鼠模型研究的信号通路。
Reactive astrocytes are associated with a vast array of central nervous system (CNS) pathologies. The activation of astrocytes is characterized by changes in their molecular and morphological features, and depending on the type of damage can also be accompanied by inflammatory responses, neuronal damage, and in severe cases, scar formation. Although reactive astrogliosis is the normal physiological response essential for containing damage, it can also have detrimental effects on neuronal survival and axon regeneration, particularly in neurodegenerative diseases. It is believed that progressive changes in astrocytes as they become reactive are finely regulated by complex intercellular and intracellular signaling mechanisms. However, these have yet to be sorted out. Much has been learned from gain-of-function approaches in vivo and culture paradigms, but in most cases, loss-of-function genetic studies, which are a critical complementary approach, have been lacking. Understanding which signaling pathways are required to control different aspects of astrogliosis will be necessary for designing therapeutic strategies to improve their beneficial effects and limit their detrimental ones in CNS pathologies. In this article, we review recent advances in the mechanisms underlying the regulation of aspects of astrogliosis, with the main focus on the signaling pathways that have been studied using loss-of-function genetic mouse models.
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影响因子：
15.3
作者：
Brambilla, R;Bracchi-Ricard, V;Hu, WH;Frydel, B;Bramwell, A;Karmally, S;Green, EJ;Bethea, JR
通讯作者：
Bethea, JR
影响因子：
5.3
作者：
Amankulor, Nduka M.;Hambardzumyan, Dolores;Holland, Eric C.
通讯作者：
Holland, Eric C.
影响因子：
6.2
作者：
Burns, Kevin A.;Murphy, Brian;Kuan, Chia-Yi
通讯作者：
Kuan, Chia-Yi
影响因子：
11.4
作者：
Brakebusch, C;Grose, R;Fässler, R
通讯作者：
Fässler, R
影响因子：
4.7
作者：
Brambilla R;Hurtado A;Persaud T;Esham K;Pearse DD;Oudega M;Bethea JR
通讯作者：
Bethea JR