抑制或基因敲除HDACs在不同视神经损伤模型中神经保护作用的研究进展

Advances in neuroprotective effects of inhibiting or gene knockout histone deacetylase in different optic nerve injury models

青光眼是导致视网膜神经节细胞(RGCs)死亡和变性的神经退行性疾病之一。据既往大量神经退行性疾病的研究表明,组蛋白去乙酰化酶(HDACs)参与细胞凋亡的早期核萎缩事件,包括组蛋白去乙酰化、异染色质形成、特异性基因的沉默以及核固缩的过程。本研究归纳总结了HDACs在不同视神经损伤模型中的研究近况,并简述了抑制或基因敲除HDACs在视神经保护分子过程中的作用。以期有助于理解HDACs在青光眼等视神经损伤疾病中的作用,为未来抑制HDACs调控RGCs存活的遗传学及分子生物学的深入研究奠定基础。

Glaucoma is one of the neurodegenerative diseases leading to death and degeneration of RGCs.According to previous studies on a large number of neurodegenerative diseases,HDACs are involved in the occurrence of nuclear atrophy in the early stage of apoptosis,including histone deacetylation,heterochromatin formation,silencing of specific genes,and nuclear pyknosis.This article summarizes the recent research of HDACs in different models of optic nerve injury and briefly describes the role of inhibiting or knocking down HDACs in molecular processes related to optic nerve protection.It is hoped to contribute to the understanding of the role of HDACs in optic nerve injury diseases such as glaucoma,and lay a foundation for further genetic and molecular biology studies on inhibiting HDACs to regulate the survival of RGCs in the future.