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

       “锌”在青光眼研究舞台上正扮演着越来越重要的角色。糖皮质激素，作为人体内重要的激素之一，其对锌的调控已在诸多系统中被证实。研究发现，在糖皮质激素的影响下，小梁网中的锌离子转运受阻，导致细胞外基质降解失衡，从而干扰小梁网正常流出道功能，加重青光眼的病情。而视神经损伤后，锌离子在神经突触间的异常传递、不平衡分布与胞内异常累积影响视网膜神经节细胞存活和轴突的再生能力，进而损害视功能，可能成为青光眼视神经损伤发病及进展的关键因素。这些研究进展为视神经保护策略提供了新的视角，“锌”作为治疗靶点的潜力正在被逐步挖掘，通过调节锌水平来干预青光眼病理进程成为可能治疗手段。
       本期封面中将汉字“锌”设计为飞天舞者，其超越时空的永恒美感，呼应了“锌”在青光眼研究中突破传统、开辟新程的角色。轻盈与自由的飞天舞者，象征着“锌”在细胞内外穿梭，精妙调控生理功能，维系细胞的和谐与平衡，为青光眼患者带来新的治疗希望。

       “锌”在青光眼研究舞台上正扮演着越来越重要的角色。糖皮质激素，作为人体内重要的激素之一，其对锌的调控已在诸多系统中被证实。研究发现，在糖皮质激素的影响下，小梁网中的锌离子转运受阻，导致细胞外基质降解失衡，从而干扰小梁网正常流出道功能，加重青光眼的病情。而视神经损伤后，锌离子在神经突触间的异常传递、不平衡分布与胞内异常累积影响视网膜神经节细胞存活和轴突的再生能力，进而损害视功能，可能成为青光眼视神经损伤发病及进展的关键因素。这些研究进展为视神经保护策略提供了新的视角，“锌”作为治疗靶点的潜力正在被逐步挖掘，通过调节锌水平来干预青光眼病理进程成为可能治疗手段。

       本期封面中将汉字“锌”设计为飞天舞者，其超越时空的永恒美感，呼应了“锌”在青光眼研究中突破传统、开辟新程的角色。轻盈与自由的飞天舞者，象征着“锌”在细胞内外穿梭，精妙调控生理功能，维系细胞的和谐与平衡，为青光眼患者带来新的治疗希望。

糖皮质激素(glucocorticoid, GC)由于其抗炎特性被广泛用于治疗眼部炎症，而G C诱导性青光眼(glucocorticoid-induced glaucoma, GIG) 作为一种常见并发症，其发病机制长期受到关注。文章综述了锌在GIG中的关键作用及其调控机制，揭示了锌在青光眼发病机制中的重要角色。锌作为人体中含量第二丰富的过渡金属，对蛋白质结构、酶催化和细胞信号调节至关重要。GC对锌分布的调控作用在不同组织和细胞类型中表现出复杂性，影响锌的摄取和释放，进而参与青光眼的病理过程。锌通过影响小梁网细胞外基质(extracellular matrix, ECM)的降解和重塑，以及视网膜神经节细胞的存活和轴突再生，在GIG的发病机制中发挥着复杂的作用。文章同时介绍了体内锌调控的现有途径，包括补充锌和减少锌的策略，提供了潜在的治疗途径。未来的研究应深入探索锌在青光眼中的作用机制以及与GC的相互作用，评估锌补充或螯合在青光眼治疗中的安全性和有效性，以及开发新型锌递送和螯合系统，有助于全面揭示锌在青光眼中的作用及治疗潜力，以实现更加精准的防治方案，改善患者预后。

Glucocorticoid (GC) is widely used in the treatment of ocular inflammation for its anti-inflammatory propery. However, glucocorticoid-induced glaucoma (GIG) is a common complication, and its pathogenesis has been extensively studied. This review summarizes the crucial role of zinc in GIG and its regulatory mechanisms, highlighting zinc's significant involvement in the pathogenesis of glaucoma. Zinc, the second most abundant transition metal in the human body, is essential for protein structure, enzyme catalysis, and cell signaling regulation. The effects of GC on zinc distribution vary across different tissues and cell types, affecting zinc uptake and release, which may contribute to the pathological processes of glaucoma. Zinc influences the degradation and remodeling of the trabecular meshwork extracellular matrix and the survival and axonal regeneration of retinal ganglion cells, playing complex roles in the pathogenesis of GIG. We discuss available strategies for regulating zinc in vivo, including zinc supplementation and reduction strategies, providing potential therapeutic approaches. Future research should explore the mechanisms of zinc's role in glaucoma and its interaction with glucocorticoids, evaluate the safety and efficacy of zinc supplementation or chelation in glaucoma treatment, and develop novel zinc delivery and chelation systems. These efforts will help fully elucidate the role of zinc in glaucoma and its therapeutic potential, enabling more precise prevention and treatment strategies to improve patient outcomes.