Traumatic spinal cord injury produces long-term neurological damage, and presents a significant public health problem with nearly 18,000 new cases per year in the U.S. The injury results in both acute and chronic changes in the spinal cord, ultimately resulting in the production of a glial scar, consisting of multiple cells including fibroblasts, macrophages, microglia, and reactive astrocytes. Within the scar, there is an accumulation of extracellular matrix (ECM) molecules—primarily tenascins and chondroitin sulfate proteoglycans (CSPGs)—which are considered to be inhibitory to axonal regeneration. In this review article, we discuss the role of CSPGs in the injury response, especially how sulfated glycosaminoglycan (GAG) chains act to inhibit plasticity and regeneration. This includes how sulfation of GAG chains influences their biological activity and interactions with potential receptors. Comprehending the role of CSPGs in the inhibitory properties of the glial scar provides critical knowledge in the much-needed production of new therapies.

创伤性脊髓损伤会产生长期的神经系统损害，并在美国每年造成近18,000例新病例，从而带来严重的公共卫生问题。损伤导致脊髓的急性和慢性变化，最终导致神经胶质的产生瘢痕，由多个细胞组成，包括成纤维细胞，巨噬细胞，小胶质细胞和反应性星形胶质细胞。在疤痕内，有大量的细胞外基质（ECM）分子（主要是肌腱蛋白和硫酸软骨素蛋白聚糖（CSPGs））积累，它们被认为可抑制轴突再生。在这篇综述文章中，我们讨论了CSPG在损伤反应中的作用，尤其是硫酸化糖胺聚糖（GAG）链如何抑制可塑性和再生。这包括GAG链的硫酸化如何影响其生物学活性以及与潜在受体的相互作用。了解CSPG在神经胶质疤痕抑制特性中的作用，为急需的新疗法生产提供了关键知识。