CNS injury often severs axons. Scar tissue that forms locally at the lesion site is thought to block axonal regeneration, resulting in permanent functional deficits. We report that inhibiting the generation of progeny by a subclass of pericytes led to decreased fibrosis and extracellular matrix deposition after spinal cord injury in mice. Regeneration of raphespinal and corticospinal tract axons was enhanced and sensorimotor function recovery improved following spinal cord injury in animals with attenuated pericyte-derived scarring. Using optogenetic stimulation, we demonstrate that regenerated corticospinal tract axons integrated into the local spinal cord circuitry below the lesion site. The number of regenerated axons correlated with improved sensorimotor function recovery. In conclusion, attenuation of pericyte-derived fibrosis represents a promising therapeutic approach to facilitate recovery following CNS injury.

中文翻译：

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减少周细胞衍生的瘢痕促进脊髓损伤后的恢复。

中枢神经系统损伤常使轴突断裂。人们认为在病变部位局部形成的瘢痕组织会阻止轴突再生，从而导致永久性功能缺陷。我们报告说，抑制子代的周细胞的产生导致小鼠脊髓损伤后纤维化和细胞外基质沉积减少。脊髓损伤后，具有减少的周细胞源性瘢痕的动物中，后踝和皮质脊髓束轴突的再生得到增强，感觉运动功能的恢复得到改善。使用光遗传学刺激，我们证明了再生的皮质脊髓束轴突整合到病变部位下方的局部脊髓回路中。再生轴突的数量与改善的感觉运动功能恢复相关。综上所述，