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Abstract：
Schwann cells respond to nerve injury by cellular reprogramming that generates cells specialized for promoting regeneration and repair. These repair cells clear redundant myelin, attract macrophages, support survival of damaged neurons, encourage axonal growth, and guide axons back to their targets. There are interesting parallels between this response and that found in other tissues. At the cellular level, many other tissues also react to injury by cellular reprogramming, generating cells specialized to promote tissue homeostasis and repair. And at the molecular level, a common feature possessed by Schwann cells and many other cells is the injury-induced activation of genes associated with epithelial-mesenchymal transitions and stemness, differentiation states that are linked to cellular plasticity and that help injury-induced tissue remodeling. The number of signaling systems regulating Schwann cell plasticity is rapidly increasing. Importantly, this includes mechanisms that are crucial for the generation of functional repair Schwann cells and nerve regeneration, although they have no or a minor role elsewhere in the Schwann cell lineage. This encourages the view that selective tools can be developed to control these particular cells, amplify their repair supportive functions and prevent their deterioration. In this review, we discuss the emerging similarities between the injury response seen in nerves and in other tissues and survey the transcription factors, epigenetic mechanisms, and signaling cascades that control repair Schwann cells, with emphasis on systems that selectively regulate the Schwann cell injury response.
摘要：
雪旺氏细胞通过细胞重编程对神经损伤作出反应，产生专门用于促进再生和修复的细胞。这些修复细胞清除多余的髓鞘，吸引巨噬细胞，支持受损神经元的存活，促进轴突生长，引导轴突回到他们的目标。这种反应与在其他组织中发现的反应之间存在有趣的相似之处。在细胞层面,许多其他组织也通过细胞重编程对损伤做出反应，产生专门促进组织稳态和修复的细胞。在分子水平上，雪旺细胞和许多其他细胞具有的共同特征是损伤诱导的与上皮-间质转化和干性相关的基因的激活，分化状态与细胞可塑性有关，并有助于损伤诱导的组织重塑。调节雪旺氏细胞可塑性的信号系统的数量正在迅速增加。重要的是,这包括对功能修复雪旺氏细胞和神经再生的产生至关重要的机制，尽管它们在施万细胞谱系的其他地方没有作用或作用较小。这鼓励了这样的观点，即可以开发选择性工具来控制这些特定的细胞，放大他们的修复支持功能，防止其恶化。在这次审查中,我们讨论了神经和其他组织中出现的损伤反应之间的相似性，并调查了转录因子，表观遗传机制，以及控制施万细胞修复的信号级联，重点是选择性调节雪旺氏细胞损伤反应的系统。
