Molecular mechanisms after optic nerve injury: Neurorepair strategies from a transcriptomic perspective.

IF 5.9 2区 医学 Q2 CELL BIOLOGY
Neural Regeneration Research Pub Date : 2026-03-01 Epub Date: 2025-04-29 DOI:10.4103/NRR.NRR-D-24-00794
Xiaxue Chen, Muyang Wei, Guangyu Li
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引用次数: 0

Abstract

Retinal ganglion cells, a crucial component of the central nervous system, are often affected by irreversible visual impairment due to various conditions, including trauma, tumors, ischemia, and glaucoma. Studies have shown that the optic nerve crush model and glaucoma model are commonly used to study retinal ganglion cell injury. While these models differ in their mechanisms, both ultimately result in retinal ganglion cell injury. With advancements in high-throughput technologies, techniques such as microarray analysis, RNA sequencing, and single-cell RNA sequencing have been widely applied to characterize the transcriptomic profiles of retinal ganglion cell injury, revealing underlying molecular mechanisms. This review focuses on optic nerve crush and glaucoma models, elucidating the mechanisms of optic nerve injury and neuron degeneration induced by glaucoma through single-cell transcriptomics, transcriptome analysis, and chip analysis. Research using the optic nerve crush model has shown that different retinal ganglion cell subtypes exhibit varying survival and regenerative capacities following injury. Single-cell RNA sequencing has identified multiple genes associated with retinal ganglion cell protection and regeneration, such as Gal , Ucn , and Anxa2 . In glaucoma models, high-throughput sequencing has revealed transcriptomic changes in retinal ganglion cells under elevated intraocular pressure, identifying genes related to immune response, oxidative stress, and apoptosis. These genes are significantly upregulated early after optic nerve injury and may play key roles in neuroprotection and axon regeneration. Additionally, CRISPR-Cas9 screening and ATAC-seq analysis have identified key transcription factors that regulate retinal ganglion cell survival and axon regeneration, offering new potential targets for neurorepair strategies in glaucoma. In summary, single-cell transcriptomic technologies provide unprecedented insights into the molecular mechanisms underlying optic nerve injury, aiding in the identification of novel therapeutic targets. Future researchers should integrate advanced single-cell sequencing with multi-omics approaches to investigate cell-specific responses in retinal ganglion cell injury and regeneration. Furthermore, computational models and systems biology methods could help predict molecular pathways interactions, providing valuable guidance for clinical research on optic nerve regeneration and repair.

视神经损伤后的分子机制:从转录组学角度看神经修复策略。
摘要:视网膜神经节细胞是中枢神经系统的重要组成部分,由于创伤、肿瘤、缺血和青光眼等各种情况,视网膜神经节细胞经常受到不可逆视力损害的影响。研究表明,视神经挤压模型和青光眼模型是研究视网膜神经节细胞损伤的常用方法。虽然这些模型的机制不同,但最终都会导致视网膜神经节细胞损伤。随着高通量技术的进步,微阵列分析、RNA测序和单细胞RNA测序等技术已被广泛应用于表征视网膜神经节细胞损伤的转录组学特征,揭示潜在的分子机制。本文就视神经损伤和青光眼模型进行综述,通过单细胞转录组学、转录组学分析和芯片分析等方法,阐明青光眼诱导视神经损伤和神经元变性的机制。视神经损伤模型的研究表明,不同的视网膜神经节细胞亚型在损伤后表现出不同的存活和再生能力。单细胞RNA测序已经鉴定出与视网膜神经节细胞保护和再生相关的多个基因,如Gal、Ucn和Anxa2。在青光眼模型中,高通量测序揭示了眼压升高下视网膜神经节细胞的转录组变化,确定了与免疫反应、氧化应激和细胞凋亡相关的基因。这些基因在视神经损伤后早期显著上调,可能在神经保护和轴突再生中起关键作用。此外,CRISPR-Cas9筛选和ATAC-seq分析已经确定了调节视网膜神经节细胞存活和轴突再生的关键转录因子,为青光眼神经修复策略提供了新的潜在靶点。总之,单细胞转录组学技术为视神经损伤的分子机制提供了前所未有的见解,有助于确定新的治疗靶点。未来的研究人员应该将先进的单细胞测序与多组学方法结合起来,研究视网膜神经节细胞损伤和再生中的细胞特异性反应。此外,计算模型和系统生物学方法可以帮助预测分子通路的相互作用,为视神经再生和修复的临床研究提供有价值的指导。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Neural Regeneration Research
Neural Regeneration Research CELL BIOLOGY-NEUROSCIENCES
CiteScore
8.00
自引率
9.80%
发文量
515
审稿时长
1.0 months
期刊介绍: Neural Regeneration Research (NRR) is the Open Access journal specializing in neural regeneration and indexed by SCI-E and PubMed. The journal is committed to publishing articles on basic pathobiology of injury, repair and protection to the nervous system, while considering preclinical and clinical trials targeted at improving traumatically injuried patients and patients with neurodegenerative diseases.
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