青光眼是全球第一大不可逆性致盲性眼病，影响全球7 000多万人，其特征是视网膜神经节细胞的退行性病变。到2040年，预计全球青光眼患者人数将增加至1.12亿，其中约10%的人至少一只眼睛失明。由高眼压诱发、多种致病因素导致的视网膜神经节细胞死亡是青光眼进展过程中视功能损伤的主要病理过程，也是青光眼病程中视功能损害不可逆的重要原因。目前降眼压治疗是唯一的干预疗法，然而其仍然不能完全遏止视网膜神经节细胞进行性损伤，并且既往病程造成的视神经损伤不可逆转。探索青光眼进程中视网膜神经节细胞退行性改变的直接致病因素，寻找关键的治疗靶点，以及开发新的具有神经保护作用的治疗药物，具有重要意义。文章回顾了近年来青光眼中视网膜神经节细胞退行性病变的机制和治疗的新进展，强调了神经血管单元的改变在青光眼发病机制中的重要作用和干预价值。同时，靶向代谢的药物应用、抑制早期炎症反应和减少氧化应激，辅以营养和运动支持等可能延缓和抑制神经退行性病变的发生，起到神经保护作用。未来青光眼发病机制的研究重点仍然在眼压之外的致病因素上，从血流、代谢和免疫串扰的病理环境中发掘对神经退行性改变重要的致病因素并进行干预治疗具有广阔的前景。在多种动物模型中验证干预手段的神经保护作用，也有望提高青光眼神经保护的临床转化成功率，以拓展青光眼的治疗理念与药物选择。

Glaucoma stands as the leading cause of irreversible blindness globally, affecting over 70 million individuals. It is characterized by progressive degeneration of retinal ganglion cells (RGCs). By 2040, the global prevalence of glaucoma is expected to rise to 112 million, with approximately 10% experiencing blindness in at least one eye. The primary pathological basis for visual function impairment in glaucoma progression is the loss of RGCs induced by elevated intraocular pressure (IOP) and various pathogenic factors. Currently, IOP-lowering treatment is the only intervention available, but it cannot completely halt the progressive injury to RGCs, nor can it reverse the optic nerve damage caused by prior disease progression. Exploring the direct pathogenic factors of RGC degeneration in glaucoma, identifying key therapeutic targets, and developing new neuroprotective treatments are of great importance. This review discusses recent advancements in the mechanisms and treatments of retinal ganglion cell degeneration in glaucoma, highlighting the significant role of neurovascular unit changes in the pathogenesis of glaucoma and the potential value of interventions. Additionally, targeting metabolites, inhibiting early inflammatory responses, and reducing oxidative stress, supplemented by nutritional and exercise support, may help delay and inhibit neurodegenerative processes, offering neuroprotective effects.Future research on glaucoma pathogenesis should focus on factors beyond IOP, exploring pathogenic factors in the pathological environment of blood flow, metabolism, and immune crosstalk for targeted therapeutic interventions. Also, verifying the neuroprotective effects of these interventions in various animal models holds promise for improving the clinical translation success rate of neuroprotection in glaucoma, thus expanding therapeutic concepts and drug options.

息肉状脉络膜血管病变(polypoidal choroidal vasculopathy,PCV)是亚洲人群中常见的致盲性眼病，发生大出血并发症后严重危害视力且预后差。PCV大出血包括视网膜下出血(subretinal hemorrhage,SRH)和玻璃体积血(vitreous hemorrhage,VH)。SRH的危险因素包括较长病程、簇型PCV、息肉状病灶不消退、合并视网膜色素上皮脱离；其治疗方式包括抗血管内皮生长因子药物、光动力疗法、激光、玻璃体腔注气、眼内注射组织纤溶酶原激活剂、玻璃体切割术或联合治疗等方式，其中，黄斑中心凹是否受累和出血时间是影响治疗方式选择的主要因素。发病年龄较大、白细胞计数较高、天门氨酸转移酶和丙氨酸转氨酶的比值较高、活化部分凝血活酶时间较长、曾行光动力疗法、有玻璃体腔注药治疗史、SRH面积大、出现视网膜色素上皮脱离的PCV患者发生VH的风险高。浓厚的VH通常需行玻璃体切割术，其手术时机和手术方式的选择是临床关注的焦点。鉴于目前PCV大出血的危险因素尚不完全明确、治疗方面也尚未形成共识，需要开展相关临床研究，提供更多依据。

Polypoidal choroidal vasculopathy (PCV) is a common blinding disease in Asian populations. Massive hemorrhage complications secondary to PCV include subretinal hemorrhage (SRH) and vitreous hemorrhage (VH). The risk factors for SRH include a long duration, clustered PCV, non-regression of polyp lesions and presented with retinal pigment epithelial detachment. The treatments for SRH include anti-vascular endothelial growth factor drugs, photodynamic therapy, laser, vitreous pneumatic displacement, intravenously injected tissue plasminogen activator, vitrectomy and combination therapy. Whether macular fovea is involved and the time since bleeding onset are the main factors afecting the choice of treatment for SRH. Older age of onset, higher white blood cell count, higher aspartate amino transferase and alanine amino transferase ratio, longer activated partial thromboplastin time retinal pigment epithelium detachment, photodynamic therapy history, intravitreal injection history larger SRH area and presented with retinal pigment epithelial detachment were associated with higher risk of VH. PCV patients with massive VH should be treated with vitrectomy, while the timing and technique of operation should be paid atention to. At present, the risk factors of PCV massive bleeding are not completely clear, and its treatment methods are diverse, which requires a large number of studies to prove its effectiveness and establish expert diagnosis and treatment consensus.

      息肉状脉络膜血管病变(polypoidal choroidal vasculopathy,PCV)是亚洲人群中常见的致盲性眼病，发生大出血并发症后严重危害视力且预后差。PCV大出血包括视网膜下出血(subretinal hemorrhage,SRH)和玻璃体积血(vitreous hemorrhage,VH)。SRH的危险因素包括较长病程、簇型PCV、息肉状病灶不消退、合并视网膜色素上皮脱离；其治疗方式包括抗血管内皮生长因子药物、光动力疗法、激光、玻璃体腔注气、眼内注射组织纤溶酶原激活剂、玻璃体切割术或联合治疗等方式，其中，黄斑中心凹是否受累和出血时间是影响治疗方式选择的主要因素。发病年龄较大、白细胞计数较高、天门氨酸转移酶和丙氨酸转氨酶的比值较高、活化部分凝血活酶时间较长、曾行光动力疗法、有玻璃体腔注药治疗史、SRH面积大、出现视网膜色素上皮脱离的PCV患者发生VH的风险高。浓厚的VH通常需行玻璃体切割术，其手术时机和手术方式的选择是临床关注的焦点。鉴于目前PCV大出血的危险因素尚不完全明确、治疗方面也尚未达成共识，需要开展相关临床研究，提供更多依据。

      息肉状脉络膜血管病变(polypoidal choroidal vasculopathy,PCV)是亚洲人群中常见的致盲性眼病，发生大出血并发症后严重危害视力且预后差。PCV大出血包括视网膜下出血(subretinal hemorrhage,SRH)和玻璃体积血(vitreous hemorrhage,VH)。SRH的危险因素包括较长病程、簇型PCV、息肉状病灶不消退、合并视网膜色素上皮脱离；其治疗方式包括抗血管内皮生长因子药物、光动力疗法、激光、玻璃体腔注气、眼内注射组织纤溶酶原激活剂、玻璃体切割术或联合治疗等方式，其中，黄斑中心凹是否受累和出血时间是影响治疗方式选择的主要因素。发病年龄较大、白细胞计数较高、天门氨酸转移酶和丙氨酸转氨酶的比值较高、活化部分凝血活酶时间较长、曾行光动力疗法、有玻璃体腔注药治疗史、SRH面积大、出现视网膜色素上皮脱离的PCV患者发生VH的风险高。浓厚的VH通常需行玻璃体切割术，其手术时机和手术方式的选择是临床关注的焦点。鉴于目前PCV大出血的危险因素尚不完全明确、治疗方面也尚未达成共识，需要开展相关临床研究，提供更多依据。