Axon growth inhibitors generated by reactive glial scars play an important role in failure of axon regeneration after CNS injury in mature mammals. Among the inhibitory factors, chondroitin sulfate proteoglycans (CSPGs) are potent suppressors of axon regeneration and are important molecular targets for designing effective therapies for traumatic brain injury or spinal cord injury (SCI). CSPGs bind with high affinity to several transmembrane receptors, including two members of the leukocyte common antigen related (LAR) subfamily of receptor protein tyrosine phosphatases (RPTPs). Recent studies demonstrate that multiple intracellular signaling pathways downstream of these two RPTPs mediate the growth-inhibitory actions of CSPGs. A better understanding of these signaling pathways may facilitate development of new and effective therapies for CNS disorders characterized by axonal disconnections. This review will focus on recent advances in the downstream signaling pathways of scar-mediated inhibition and their potential as the molecular targets for CNS repair.

由反应性神经胶质瘢痕产生的轴突生长抑制剂在成熟哺乳动物中枢神经系统损伤后的轴突再生失败中起重要作用。在抑制因素中，硫酸软骨素蛋白聚糖（CSPG）是轴突再生的有效抑制剂，并且是设计用于治疗颅脑损伤或脊髓损伤（SCI）的有效疗法的重要分子靶标。CSPG以高亲和力与几种跨膜受体结合，包括受体蛋白酪氨酸磷酸酶（RPTP）的白细胞共同抗原相关（LAR）亚家族的两个成员。最近的研究表明，这两个RPTP下游的多个细胞内信号传导途径介导CSPG的生长抑制作用。对这些信号通路的更好理解可能有助于开发以轴突断开为特征的中枢神经系统疾病的新的有效疗法。这项审查将侧重于疤痕介导的抑制作用的下游信号通路的最新进展及其作为中枢神经系统修复分子靶标的潜力。