创伤性脊髓损伤后的蛋白质乙酰化：机制与治疗机遇
The Protein Acetylation after Traumatic Spinal Cord Injury: Mechanisms and Therapeutic Opportunities.
作者信息
Li Hong-Wei, Zhang Hai-Hong
机构信息
Department of Spine Surgery, Lanzhou University Second Hospital; Orthopaedics Key Laboratory of Gansu Province, Lanzhou 730030, China.
出版信息
Int J Med Sci. 2024 Feb 12;21(4):725-731. doi: 10.7150/ijms.92222. eCollection 2024.
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.
脊髓损伤（SCI）会导致各种正常功能的缺陷，且难以恢复到正常状态。SCI后的组蛋白和非组蛋白乙酰化已有充分记载，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。在本综述中，我们总结了目前关于组蛋白和非组蛋白乙酰化在调节SCI中神经元生长和轴突再生作用的研究。此外，我们讨论了靶向乙酰化相关酶的抑制剂和激活剂，如α-微管蛋白乙酰转移酶1（αTAT1）、组蛋白去乙酰化酶6（HDAC6）和沉默调节蛋白2（SIRT2），为SCI的恢复提供了有前景的机会。总之，全面了解SCI中的蛋白质乙酰化和去乙酰化可能有助于SCI治疗的发展。
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