ROCKing Regeneration: Rho Kinase Inhibition as Molecular Target for Neurorestoration.
ROCKing Regeneration: Rho Kinase Inhibition as Molecular Target for Neurorestoration.
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DOI：
10.3389/fnmol.2011.00039
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发表时间：
2011
影响因子：
4.8
通讯作者：
Lingor P
中科院分区：
文献类型：
--
作者：
Tönges L;Koch JC;Bähr M;Lingor P
中枢神经系统的再生失败很大程度上取决于病变刺激后明显的生长抑制信号和细胞存活减少。生长抑制信号的一个关键介质是rho相关激酶（ROCK），它已被证明通过调节肌动蛋白动力学来调节生长锥的稳定性。最近，越来越多的证据表明，ROCK对细胞存活也起着有害的作用。在这篇文章中，我们说明ROCK参与了多种细胞内信号通路，这些信号通路远远超过了单独参与神经突生长抑制的信号通路。虽然ROCK功能目前在许多不同的疾病背景下被研究，但我们的综述主要集中在中枢神经系统的神经修复方法，特别是在神经创伤模型中。通过药理小分子抑制剂和RNAi方法靶向ROCK的有希望的策略在临床前和临床研究中评估了它们在再生生长和细胞保护方面的结果。
Regenerative failure in the CNS largely depends on pronounced growth inhibitory signaling and reduced cellular survival after a lesion stimulus. One key mediator of growth inhibitory signaling is Rho-associated kinase (ROCK), which has been shown to modulate growth cone stability by regulation of actin dynamics. Recently, there is accumulating evidence the ROCK also plays a deleterious role for cellular survival. In this manuscript we illustrate that ROCK is involved in a variety of intracellular signaling pathways that comprise far more than those involved in neurite growth inhibition alone. Although ROCK function is currently studied in many different disease contexts, our review focuses on neurorestorative approaches in the CNS, especially in models of neurotrauma. Promising strategies to target ROCK by pharmacological small molecule inhibitors and RNAi approaches are evaluated for their outcome on regenerative growth and cellular protection both in preclinical and in clinical studies.
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