Optic nerve damage as a result of trauma, ischemia, glaucoma or other forms of optic neuropathy disease, leads to disconnection between the eye and brain and death of retinal ganglion cells (RGCs), causing permanent loss of vision. Therapeutic options for treating optic neuropathy are limited and represent a significant unmet medical need. Development of a regenerative strategy for replacement of lost RGCs lies at the core of the future cell-based therapy for these conditions. Successful long-term restoration of visual function depends on the type of cells for transplantation. Primary RGCs of neonatal mice are now reported to have the potential for serving such a purpose.

Optic nerve damage as a result of trauma, ischemia, glaucoma or other forms of optic neuropathy disease, leads to disconnection between the eye and brain and death of retinal ganglion cells (RGCs), causing permanent loss of vision. Therapeutic options for treating optic neuropathy are limited and represent a significant unmet medical need. Development of a regenerative strategy for replacement of lost RGCs lies at the core of the future cell-based therapy for these conditions. Successful long-term restoration of visual function depends on the type of cells for transplantation. Primary RGCs of neonatal mice are now reported to have the potential for serving such a purpose.

Purpose: To investigate the effect of intravitreal injection of basic fibroblast growth factor (bFGF) on activation and proliferation of endogenous retinal progenitor cells in the Royal College of Surgeons (RCS) rat.

Methods: Twenty-four rats were studied after the 30th postnatal day (≥30). Eighteen RCS-p⁺/LAV rats were divided into 3 groups: bFGF-treated, vehicle-treated, and untreated groups randomly, and 6 RCS-ray⁺p⁺/Lav rats were used as normal controls. 6 μl of bFGF (5 μg /10 μl) or vehicle was injected into the vitreous on day 31, 33, and 35 after birth (P31, P33, P35) in the bFGF group and vehicle group respectively, and no injections were administered in the untreated and control groups. All the rats were euthanized, and their eyes were enucleated, hemisected, and fixed at 50 days after birth for immunohistochemistry and measurement of outer nuclear layer thickness.

Results: Nestin and Chx10 were positive in all retinal layers. Intravitreal injection of bFGF in retina-dystrophic RCS (RCS-p⁺/Lav) rats induced intense labeling for the retinal progenitor cell markers Chx10 and Nestin, which were highly colocalized. Fluorescence intensity for both labels was somewhat less in the control rats, and much less in the vehicle-injected rats as well as in the untreated RCS rats. The outer nuclear layer (ONL) was significantly thicker in the bFGF group than that in the vehicle-treated or untreated group (P < 0.01), but thinner than that of the control group (P < 0.01). No significant difference was observed in the ONL thickness between the vehicle group and untreated group (P > 0.05).

Conclusion: bFGF may contribute to the activation of retinal progenitor cells in RCS rats, thus counteracting degeneration by promoting the proliferation of the progenitor cells.

Purpose: To investigate the effect of intravitreal injection of basic fibroblast growth factor (bFGF) on activation and proliferation of endogenous retinal progenitor cells in the Royal College of Surgeons (RCS) rat.

Methods: Twenty-four rats were studied after the 30th postnatal day (≥30). Eighteen RCS-p⁺/LAV rats were divided into 3 groups: bFGF-treated, vehicle-treated, and untreated groups randomly, and 6 RCS-ray⁺p⁺/Lav rats were used as normal controls. 6 μl of bFGF (5 μg /10 μl) or vehicle was injected into the vitreous on day 31, 33, and 35 after birth (P31, P33, P35) in the bFGF group and vehicle group respectively, and no injections were administered in the untreated and control groups. All the rats were euthanized, and their eyes were enucleated, hemisected, and fixed at 50 days after birth for immunohistochemistry and measurement of outer nuclear layer thickness.

Results: Nestin and Chx10 were positive in all retinal layers. Intravitreal injection of bFGF in retina-dystrophic RCS (RCS-p⁺/Lav) rats induced intense labeling for the retinal progenitor cell markers Chx10 and Nestin, which were highly colocalized. Fluorescence intensity for both labels was somewhat less in the control rats, and much less in the vehicle-injected rats as well as in the untreated RCS rats. The outer nuclear layer (ONL) was significantly thicker in the bFGF group than that in the vehicle-treated or untreated group (P < 0.01), but thinner than that of the control group (P < 0.01). No significant difference was observed in the ONL thickness between the vehicle group and untreated group (P > 0.05).

Conclusion: bFGF may contribute to the activation of retinal progenitor cells in RCS rats, thus counteracting degeneration by promoting the proliferation of the progenitor cells.

目的：研究玻璃体腔注射曲安奈德(triamcinolone acetonide,TA)和雷珠单抗(Lucentis)治疗视网 膜中央静脉阻塞(central retinal vein occlusion,CRVO)的黄斑水肿的疗效。方法：配对病例对照研究。将2013年1月至2015年6月，在我院因CRVO并发黄斑水肿而接受玻璃体腔注射TA或Lucentis 的患者，根据患者基线水平的最佳矫正视力(best-corrected visual acuity,BCVA)(logMAR视力)和黄斑中心厚度(central macular thickness,CMT)将两组患者进行配对，选出12对患者，主要的观察 指标为随访1年时两组患者的BCVA和CMT。结果：TA组患者的BCVA由基线时的0.78±0.12提高到 0.55±0.24(P=0.005),CMT由基线时的(598.92±192.67) μm减少到(258.28±75.38) μm (P=0.002)。Lucentis组患者的BCVA由基线时的0.78±0.11提高到0.48±0.21(P=0.002), CMT由基线时的 (591.75±181.68) μm减少到(281.17±63.08) μm (P=0.002)。TA组和Lucentis组患者基线及最终的 BCVA和CMT直接均无显著差异。TA组的平均注药次数为(2.4±0.9)次，Lucentis组为(4.0±1.6)次， 两组有统计学差异(P=0.012)。结论：玻璃体腔注射TA或Lucentis均能减轻CRVO所致的黄斑水肿并提高视力，两者的疗效并无显著差异。TA的平均注射次数比Lucentis组少，但是TA更容易引起眼压升高。应该根据患者的综合情况制定个性化的治疗方案。

Objective: To compare the efficacy of intravitreal injections of triamcinolone acetonide (TA) and that of ranibizumab for macular edema secondary to central retinal vein occlusion (CRVO). Methods: In a retrospective assessment 12 TA-treated patients and 12 ranibizumab-treated ones with macular edema after CRVO were pairmatched according to initial best-corrected visual acuity (BCVA) and central macular thickness (CMT). BCVA and CMT were the main endpoints. Results: The initial BCVA of 0.78±0.12 increased significantly to 0.55±0.24 in the TA-treated patients (P=0.005). And the initial CMT of (598.92±192.67) μm decreased significantly to (258.28±75.38) μm (P=0.002). In the ranibizumab-treated patients, the initial BCVA of 0.78±0.11 increased significantly to 0.48±0.21 (P=0.002) and the initial CMT of (591.75±181.68) μm decreased significantly to (281.17±63.08) μm (P=0.002). There was no significance between the initial and final BCVA and CMT of TAtreated patients and ranibizumab-treated patients. Conclusion: Both treatments decreased the CMT and induced an improvement in BCVA from baseline.

目的: 分析高度近视眼行白内障摘除及后房型人工晶状体植入术后并发裂孔源性视网膜脱离的发生率、相关危险因素及临床特点。

方法 : 回顾性分析高度近视眼行白内障摘除及后房型人工晶状体植入术患者 146 例(232 只眼) 。裂孔源性视网膜脱离在术后随访的3年时间发生。所有眼均进行了详细的眼科检查, 包括: 最佳矫正视力、眼底检查、A 超眼轴长度测量。

结果: 15 只眼发生裂孔源性视网膜脱离(6.4%) , 均需行玻璃体视网膜手术进行视网膜复位。从白内障手术到发生视网膜脱离的平均时间为10 ± 9 个月(0.5～32 个月) 。视网膜脱离经手术治疗后视力为手动 /10 cm～0.06, 12 只眼(80%) 最终视力低于白内障术前。术中后囊膜破裂与术后视网膜脱离的发生显著相关 (P < 0.01) , 60%(9/15) 的视网膜脱离患者术中发生了后囊膜破裂。

结论: 高度近视眼白内障术后并发裂孔源性视网膜脱离的发生率为 6.4%, 其预后差。术中发生后囊膜破裂患者术后发生视网膜脱离的危险性更高, 对术中后囊膜破裂患者需密切随访。

Aim: To analyze the clinical characteristics, incidence and risk of retinal detachment (RD) after cataract surgery and posterior chamber intraocular lens implantation in high myopic patients.

Methods:The medical records of 146 high myopic patients (232 eyes) who underwent cataract surgery and posterior chamber intraocular lens implantation were studied retrospectively. The development of RD was followed up over a 3-year period, and its characteristics were determined. All of the eyes received a comprehensive ophthal-mological examination, including best-corrected visual acuity measurements, a dilated fundus examination and axial length measured by A-scan ultrasonography.

Results: RD developed in 15 eyes of 15 patients. All the 15 eyes needed vitreo-retinal surgery. The mean interval between cataract surgery and the development of RD was 10 ± 9 months (range 0.5～32 months) . The visual results of the eyes after anatomical successful vitreo-retinal surgery ranged from finger count /10 cm to 0.06. 80% (12/15) of the eyes had a worse vision after the surgery than that before cataract surgery. Posterior capsular tear were associated significantly with RD (P < 0.01). Approximately 60%( 9/15) of retinal detachment was attributable to posterior capsule tear during cataract surgery.

Conclusion: Incidence of RD in high myopic patients after cataract surgery was 6.4%. RD was the potentially serious complication and tended to develop more frequently in eyes with posterior capsular rupture during cataract surgery. It is crucial to examine retinal status after cataract surgery and to have a close follow-up to prevent retinal complications, especially for patients with posterior capsular disruption. 

铁死亡是一种以铁沉积和脂质过氧化为主要特征的新型细胞死亡方式，目前在眼科方面的研究不断深入。视网膜因其本身功能和结构特点，易受到氧化应激的影响，而铁死亡已被证明在年龄相关性黄斑变性、青光眼、糖尿病性视网膜病变、视网膜色素变性等视网膜退行性疾病进程中发挥了重要作用。铁代谢途径作为铁死亡的主要调控方式之一，可通过调控细胞内铁稳态，介导芬顿反应形成脂质过氧化物，从而调控细胞铁死亡。转铁蛋白(transferrin,TF)、二价金属转运蛋白1(divalent metal transporter 1,DMT1)、铁蛋白(ferritin,FT)、铁转运蛋白1(ferroportin 1,FPN1)等铁代谢途径关键蛋白涉及细胞内铁离子的摄入、利用、储存、输出等多个方面，对细胞内铁稳态具有重要影响。通过调控铁代谢途径关键蛋白减少铁沉积而抑制铁死亡，可能成为延缓和治疗视网膜退行性疾病的新途径。文章对铁死亡概念、视网膜与铁死亡、铁死亡调控途径、铁代谢途径关键蛋白与视网膜退行性疾病的研究进展进行综述。

Ferroptosis, a novel form of cell death primarily characterized by iron deposition and lipid peroxidation, has been increasingly studied in the feld of ophthalmology. Te retina, due to its specifc functions and structure, is susceptible to oxidative stress. Ferroptosis has been proven to play a crucial role in the progression of retinal degenerative diseases such as age-related macular degeneration, glaucoma, diabetic retinopathy, and retinitis pigmentosa. Te iron metabolism pathway is one of the main regulatory mechanisms of ferroptosis, regulating intracellular iron homeostasis and mediating the formation of lipid peroxides through the Fenton reaction, thereby controlling cellular ferroptosis. Iron metabolism pathways, as one of the main regulatory mechanisms of ferroptosis, can regulate intracellular iron homeostasis and mediate the formation of lipid peroxides through the Fento reaction, thereby controlling cellur ferroptosis. Key proteins involved in iron metabolism pathways, including transferrin (TF), divalent metal transporter 1 (DMT1), ferritin (FT), and ferroportin 1 (FPN1), act as important roles in various aspects such as intracellular iron intake, utilization, storage, and export, exerting signifcant impacts on intracellular iron homeostasis. Regulating key proteins in iron metabolism pathways to reduce iron deposition and inhibiting ferroptosis may emerge aas a novel approach for delaying and treating retinal degenerative diseases. Tis article provides a comprehensive review of the concept of ferroptosis, the relationship between the retina and ferroptosis, the regulatory mechanisms of ferroptosis, and the research progress on key proteins in iron metabolism pathways and retinal degenerative diseases.

年龄相关性黄斑变性(age-related macular degeneration,AMD)是一种发生在黄斑区的退行性变，其中湿性年龄相关性黄斑变性(wet age-related macular degeneration,wAMD)以黄斑区新生血管为主要病理特征，是导致老年人视力受损甚至失明的重要原因，视网膜下纤维化是wAMD最常见的自然后遗症，可导致光感受器、视网膜色素上皮(retinal pigment epithelial,RPE)和脉络膜毛细血管受损，导致不可逆转的中心视力丧失。多种基线特征被发现是视网膜下纤维化的危险因素，可用于预测早期视网膜下纤维化的发生。迄今为止，还没有有效的抗纤维化治疗方法，抗血管内皮生长因子(anti-vascular endothelia growth factor, anti-VEGF)治疗是wAMD的一线治疗方案，该治疗方法不能改善视网膜下纤维化，但及时启动治疗可能有助于预防或延缓纤维化的进展，目前多种靶向分子药物正被研发用于抗纤维化的治疗。该文综述了wAMD视网膜下纤维化的临床表现及意义、预测纤维化形成的基线特征、基本发病机制及潜在的抗纤维化治疗方法，旨在为临床诊治工作提供参考。

Age-related macular degeneration (AMD) is a degenerative disease of the macular, and wet age-related macular degeneration(wAMD) is mainly characterized by macular neovascularization, which is an important reason of visual impairment or even blindness in the elderly. Subretinal fibrosis is the most common natural sequelae of wAMD, which can lead to irreversible central vision loss by damaging photoreceptors, RPE, and choroidal capillaries. Multiple baseline features have been identified as the risk factors for subretinal fibrosis, which can be used to predict the early subretinal fibrosis. Heretofore, no anti fibrotic treatment method is effective. Anti vascular endothelial growth factor (anti VEGF) treatment is the first-line treatment for wAMD. This therapy cannot improve subretinal fibrosis, but timely initiation of treatment may help prevent or delay the progression of fibrosis. Currently, multiple targeted molecular drugs are being developed for anti fibrotic treatment. This article reviews the clinical manifestations and significance of subretinal fibrosis in wet age-related macular degeneration, baseline features for predicting the formation of fibrosis, basic pathogenesis, and potential anti-fibrosis treatment methods,aiming to provide reference for clinical diagnosis and treatment.

孔源性视网膜脱离(rhegmatogenous retinal detachment,RRD)是一种严重威胁视力的眼部疾病，目前治疗手段以手术为主，手术方式主要有视网膜气体填充术(pneumatic retinopexy,PR)、巩膜扣带术(scleral buckling,SB)以及经睫状体扁平部玻璃体切割术(pars plana vitrectomy,PPV)。目前对于RRD手术术式的选择仍然存在争议，因此研究及制定RRD手术方式抉择的临床策略具有重要的临床意义。而临床上制定RRD患者手术方案往往与患者的年龄、视网膜脱离时间、裂孔的类型、位置、数量、大小等等临床因素有关，该文就影响孔源性视网膜脱离手术抉择的相关临床因素进行综述。

Rhegmatogenous retinal detachment (RRD) is a serious eye disease threatening vision. Surgery is main treatment currently, and surgery approaches include pneumatic retinopexy (PR), scleral buckling (SB), and pars plana vitrectomy(PPV). There is still controversy over the selection of RRD surgery approaches, so it is great significant to study and develop clinical strategies for RRD surgery approaches. The surgical plans for RRD patients are often related to clinical factors, such as the patient’s age, retinal detachment time, type, location, quantity, size, etc. This article reviews the related clinical factors affecting the surgical decision for rhegmatogenous retinal detachment.