Retinal ganglion cells (RGCs) extend through the optic nerve, connecting with neurons in visually related nuclei. Similar to most mature neurons in the central nervous system, once damaged, RGCs are unable to regenerate their axons and swiftly progress to cell death. In addition to cell-intrinsic mechanisms, extrinsic factors within the extracellular environment, notably glial and inflammatory cells, exert a pivotal role in modulating RGC neurodegeneration and regeneration. Moreover, burgeoning evidence suggests that retinal interneurons, specifically amacrine cells, exert a substantial influence on RGC survival and axon regeneration. In this review, we consolidate the present understanding of extrinsic factors implicated in RGC survival and axon regeneration, and deliberate on potential therapeutic strategies aimed at fostering optic nerve regeneration and restoring vision.

Retinal ganglion cells (RGCs) extend through the optic nerve, connecting with neurons in visually related nuclei. Similar to most mature neurons in the central nervous system, once damaged, RGCs are unable to regenerate their axons and swiftly progress to cell death. In addition to cell-intrinsic mechanisms, extrinsic factors within the extracellular environment, notably glial and inflammatory cells, exert a pivotal role in modulating RGC neurodegeneration and regeneration. Moreover, burgeoning evidence suggests that retinal interneurons, specifically amacrine cells, exert a substantial influence on RGC survival and axon regeneration. In this review, we consolidate the present understanding of extrinsic factors implicated in RGC survival and axon regeneration, and deliberate on potential therapeutic strategies aimed at fostering optic nerve regeneration and restoring vision

青光眼是一种以视网膜神经节细胞(retinal ganglion cell, RGC)及其轴突的进行性变性和丢失为主要特征的眼病，是导致视力丧失的最常见原因。尽管其具体的发病机制尚未完全明确，但众所周知，眼内压升高是青光眼进展的主要危险因素。目前，通过药物和手术治疗降低眼内压是控制疾病进展的主要手段。他氟前列素因其能有效长期稳定地降低眼内压，且不良反应轻微、患者依从性高、无明显全身不良反应，已成为治疗原发性开角型青光眼及眼高压症的一线治疗药物。近年来的研究表明，他氟前列素除了具有降低眼内压的效果外，还可能具有神经保护作用。文章对他氟前列素的药理作用及其在神经保护方面的潜在效益进行综述，为开发更有效的治疗青光眼药物提供理论依据和科研基础。然而，目前缺乏充分的临床研究证据支持其神经保护效应，未来研究应进一步探索这一领域，以促进针对视神经保护的药物开发和基于视神经再生的视觉功能重建。

Glaucoma is characterized by the progressive degeneration and loss of retinal ganglion cells (RGC) and their axons,making it one of the most common causes of vision loss. Although the exact underlying mechanisms remain unclear, it is well known that elevated intraocular pressure (IOP) is a major risk factor for the progression of glaucoma. Currently, the primary means of controlling glaucoma involves reducing IOP through medication and surgery. Tafluprost, due to its effective and long-term ability to lower IOP, minimal side effects, high patient compliance, and absence of significant systemic side effects, has become the first-line treatment for primary open-angle glaucoma and ocular hypertension. Recent studies suggest that tafluprost may also have neuroprotective effects beyond its IOP-lowering effects. This article aims to review the pharmacological and potential neuroprotective effects of tafluprost, providing a theoretical basis and research foundation for developing more effective drugs for glaucoma treatment. However, there is still a lack of sufficient clinical evidence to support the neuroprotective effects of tafluprost, and further investigations are required to explore in this field to furnish critical theoretical backing for the development of drugs that target optic nerve protection and facilitate vision restoration through optic nerve regeneration.