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Abstract：
Spinal cord injury (SCI) leads to deficits of various normal functions and is difficult to return to a normal state. Histone and non-histone protein acetylation after SCI is well documented and regulates spinal cord plasticity, axonal growth, and sensory axon regeneration. However, our understanding of protein acetylation after SCI is still limited. In this review, we summarize current research on the role of acetylation of histone and non-histone proteins in regulating neuron growth and axonal regeneration in SCI. Furthermore, we discuss inhibitors and activators targeting acetylation-related enzymes, such as α-tubulin acetyltransferase 1 (αTAT1), histone deacetylase 6 (HDAC6), and sirtuin 2 (SIRT2), to provide promising opportunities for recovery from SCI. In conclusion, a comprehensive understanding of protein acetylation and deacetylation in SCI may contribute to the development of SCI treatment.
摘要：
脊髓损伤（SCI）导致各种正常功能的缺陷，并且难以恢复正常状态。SCI后组蛋白和非组蛋白蛋白乙酰化是有据可查的，并调节脊髓可塑性，轴突生长,和感觉轴突再生。然而,我们对SCI后蛋白质乙酰化的理解仍然有限.在这次审查中,本文综述了组蛋白和非组蛋白蛋白乙酰化在脊髓损伤中对神经元生长和轴突再生的调控作用。此外，我们讨论了针对乙酰化相关酶的抑制剂和活化剂，如α-微管蛋白乙酰转移酶1（αTAT1），组蛋白脱乙酰酶6（HDAC6），和沉默蛋白2(SIRT2)，为从SCI恢复提供有希望的机会。总之,对SCI中蛋白质乙酰化和脱乙酰化的全面了解可能有助于SCI治疗的发展。
