Wang Xingyu, Luo Huiyu
Department of Anesthesiology, Xiangyang No 1 People's Hospital Affiliated to Hubei University of Medicine, Xiangyang 441000, China.
Department of Anesthesiology, Xiangyang No 1 People's Hospital Affiliated to Hubei University of Medicine, Xiangyang 441000, China.
Pharmacol Res. 2025 Jul;217:107813. doi: 10.1016/j.phrs.2025.107813. Epub 2025 Jun 13.
Histone acetylation is currently one of the epigenetic mechanisms that have been extensively and profoundly studied, and is associated with the occurrence and development of various diseases such as cancer and neurodegenerative disorders.Histone acetylation/deacetylation refers to the addition/removal of acetyl groups on histone lysine residues under the action of histone acetyltransferase (HAT)/histone deacetylase (HDAC), and is read by BET proteins, influencing gene transcription. In recent years, an increasing amount of evidence has indicated that histone acetylation plays a vital role in neuropathic pain. Neuropathic pain is an unresolved medical issue for which no effective treatment measures are available.Therefore, This article, from a novel perspective of HAT, HDAC, and BET proteins, deeply exploresthe mechanism of histone acetylation in various neuropathic pain models. The study found that HAT, HDAC, and BET proteins,at multiple levels, affect the expression of proteins such as ion channels, chemokines.and inflammatory factors through gene regulatory mechanisms. Based on this, future research can focus on the drug development targeting HAT, HDAC, and BET proteins, with the expectation of achieving more precise and effective regulation of neuropathic pain at the genetic level.
组蛋白乙酰化是目前已被广泛深入研究的表观遗传机制之一，并且与癌症和神经退行性疾病等各种疾病的发生发展相关。组蛋白乙酰化/去乙酰化是指在组蛋白乙酰转移酶（HAT）/组蛋白去乙酰化酶（HDAC）的作用下，组蛋白赖氨酸残基上乙酰基的添加/去除，并由BET蛋白识别，影响基因转录。近年来，越来越多的证据表明组蛋白乙酰化在神经性疼痛中起着至关重要的作用。神经性疼痛是一个尚未解决的医学问题，目前尚无有效的治疗措施。因此，本文从HAT、HDAC和BET蛋白这一新的角度，深入探讨了组蛋白乙酰化在各种神经性疼痛模型中的机制。研究发现，HAT、HDAC和BET蛋白通过基因调控机制在多个水平上影响离子通道、趋化因子和炎症因子等蛋白质的表达。基于此，未来的研究可以聚焦于针对HAT、HDAC和BET蛋白的药物开发，期望在基因水平上实现对神经性疼痛更精确有效的调控。
