A major consequence of traumatic brain and spinal cord injury is the loss of the myelin sheath, a cholesterol-rich layer of insulation that wraps around axons of the nervous system. In the central nervous system (CNS), myelin is produced and maintained by oligodendrocytes. Damage to the CNS may result in oligodendrocyte cell death and subsequent loss of myelin, which can have serious consequences for functional recovery. Demyelination impairs neuronal function by decelerating signal transmission along the axon and has been implicated in many neurodegenerative diseases. After a traumatic injury, mechanisms of endogenous remyelination in the CNS are limited and often fail, for reasons that remain poorly understood. One area of research focuses on enhancing this endogenous response. Existing techniques include the use of small molecules, RNA interference (RNAi), and monoclonal antibodies that target specific signaling components of myelination for recovery. Cell-based replacement strategies geared towards replenishing oligodendrocytes and their progenitors have been utilized by several groups in the last decade as well. In this review article, we discuss the effects of traumatic injury on oligodendrocytes in the CNS, the lack of endogenous remyelination, translational studies in rodent models promoting remyelination, and finally human clinical studies on remyelination in the CNS after injury.

创伤性脑和脊髓损伤的一个主要后果是髓鞘的丧失，髓鞘是包裹神经系统轴突的富含胆固醇的绝缘层。在中枢神经系统 (CNS) 中，髓磷脂由少突胶质细胞产生和维持。中枢神经系统损伤可能导致少突胶质细胞死亡和随后的髓鞘质丧失，这可能对功能恢复产生严重后果。脱髓鞘通过减慢沿轴突的信号传输来损害神经元功能，并且与许多神经退行性疾病有关。创伤性损伤后，中枢神经系统内源性髓鞘再生机制受到限制，并且经常失败，其原因仍知之甚少。研究领域的一个重点是增强这种内源性反应。现有技术包括使用小分子、RNA 干扰 (RNAi) 和单克隆抗体，针对髓鞘形成的特定信号成分进行恢复。在过去的十年中，一些研究小组也采用了旨在补充少突胶质细胞及其祖细胞的基于细胞的替代策略。在这篇综述文章中，我们讨论了创伤性损伤对中枢神经系统少突胶质细胞的影响、内源性髓鞘再生的缺乏、促进髓鞘再生的啮齿动物模型的转化研究，以及受伤后中枢神经系统髓鞘再生的人类临床研究。