Regeneration is bungled following CNS injuries, including spinal cord injury (SCI). Inherent decay of permissive conditions restricts the regrowth of the mature CNS after an injury. Hypertrophic scarring, insignificant intrinsic axon-growth activity, and axon-growth inhibitory molecules such as myelin inhibitors and scar inhibitors constitute a significant hindrance to spinal cord repair. Besides these molecules, a combined absence of various mechanisms responsible for axonal regeneration is the main reason behind the dereliction of the adult CNS to regenerate. The neutralization of specific inhibitors/proteins by stymieing antibodies or encouraging enzymatic degradation results in improved axon regeneration. Previous efforts to induce regeneration after SCI have stimulated axonal development in or near lesion sites, but not beyond them. Several pathways are responsible for the axonal growth obstruction after a CNS injury, including SCI. Herein, we summarize the axonal, glial, and intrinsic factor which impedes the regeneration. We have also discussed the methods to stabilize microtubules and through this to maintain the proper cytoskeletal dynamics of growth cone as disorganized microtubules lead to the failure of axonal regeneration. Moreover, we primarily focus on diverse inhibitors of axonal growth and molecular approaches to counteract them and their downstream intracellular signaling through the RhoA/ROCK pathway.

中枢神经系统损伤（包括脊髓损伤 (SCI)）后，再生会受到阻碍。允许条件的固有衰减限制了受伤后成熟中枢神经系统的再生。肥厚性瘢痕形成、不显着的内在轴突生长活性和轴突生长抑制分子如髓鞘抑制剂和瘢痕抑制剂构成了脊髓修复的显着障碍。除了这些分子之外，负责轴突再生的各种机制的联合缺失是成人中枢神经系统无法再生的主要原因。通过阻碍抗体或促进酶促降解来中和特定抑制剂/蛋白质可改善轴突再生。先前在 SCI 后诱导再生的努力刺激了损伤部位内或附近的轴突发育，但不会超出它们。包括 SCI 在内的 CNS 损伤后轴突生长受阻的原因有多种。在此，我们总结了阻碍再生的轴突、神经胶质和内在因素。我们还讨论了稳定微管的方法，并通过这种方法来维持生长锥的适当细胞骨架动力学，因为微管无序会导致轴突再生失败。此外，我们主要关注轴突生长的多种抑制剂和通过 RhoA/ROCK 途径抵消它们及其下游细胞内信号传导的分子方法。我们还讨论了稳定微管的方法，并通过这种方法来维持生长锥的适当细胞骨架动力学，因为微管无序会导致轴突再生失败。此外，我们主要关注轴突生长的多种抑制剂和通过 RhoA/ROCK 途径抵消它们及其下游细胞内信号传导的分子方法。我们还讨论了稳定微管的方法，并通过这种方法来维持生长锥的适当细胞骨架动力学，因为微管无序会导致轴突再生失败。此外，我们主要关注轴突生长的多种抑制剂和通过 RhoA/ROCK 途径抵消它们及其下游细胞内信号传导的分子方法。