作者：戴珊珊 陈小美
美工：何国红 罗真真
排版：马超
眼睛是人体最重要的感官器官，负责感知超过80%的外部信息。眼睛的健康不仅关系到人的生活质量，也是国家人口健康状况的重要指标。然而，世界卫生组织(WHO)的数据表明，全球最少有22亿人患有视力障碍或失明，其中至少有10亿病例是可以预防或治疗的，眼科疾病防治已经迫在眉睫。
▲ 图1. 常见疾病视力障碍常见原因的位置和临床表现
当前眼科疾病谱系广泛，其中屈光不正、结膜炎等患者基数庞大，白内障与青光眼是主要的致盲病因，而视网膜病变与甲状腺相关眼病则因机制复杂、预后不佳，构成了当前诊疗的重点与难点。目前诊疗策略上，已形成光学矫正、手术干预与药物疗法相结合的多元化体系。然而随着对眼免疫炎症机制认识的深化及抗体药物研发的突破，治疗模式已从抗VEGF药物引领的靶向治疗，逐步迈向系统免疫调控与局部精准干预并重的新阶段，标志着眼科进入精准化与系统化并进的诊疗时代。
▼ 表1 常见眼科疾病汇总
01 年龄相关性黄斑变性（AMD）：老年致盲“头号元凶”
01
疾病分类及发病率
年龄相关性黄斑变性（Age-related macular degeneration，AMD）主要累及视网膜黄斑区的退行性眼底疾病，分为干性（地图样萎缩型，geographic atrophy，GA）和湿性（新生血管型，Neovascular age-related macular degeneration，nAMD）两大亚型，前者占比90%，后者虽仅占10%，却是导致严重视力丧失的主因。65岁以上人群发病率显著升高（北美/欧洲达10%），90岁以上人群发病率超36.7/1000；干性AMD早期无症状，晚期因光感受器细胞丢失致中心视野缺损，nAMD因脉络膜新生血管（Choroidal neovascularization，CNV）渗漏，短期内可致失明。
2020年全球AMD患者1.96亿，2040年将飙升至2.88亿；美国2019年已有2000万患者，其中150万为晚期重症，欧洲裔患病率（12.33%）显著高于亚裔（7.38%）、非洲裔（7.53%）。
02
致病机制
干性AMD：慢性低度炎症+补体系统过度激活，视网膜下出现玻璃膜疣、视网膜下沉积物（SDD），逐步导致视网膜色素上皮（RPE）细胞与光感受器变性萎缩。
湿性AMD：炎症、缺氧等触发血管新生，肥大细胞、巨噬细胞释放血管内皮生长因子（VEGF），打破VEGF与色素上皮衍生因子（PEDF）平衡，异常CNV突破Bruch膜，引发渗漏、出血与瘢痕。
▲ 图 2：年龄相关性黄斑变性（AMD）发病机制
03
已上市治疗方案与药物
对这些关键病理机制的深入理解，直接推动了靶向治疗药物的开发。当前的治疗策略正致力于精准干预上述通路：通过抑制VEGF来控制湿性AMD的异常血管生长，或通过调节补体通路来延缓干性AMD的进展。目前已上市的代表性药物如下：
▼ 表2 AMD治疗方案与药物
04
热门在研靶点与新兴疗法
1) VEGF通路：布西珠单抗 (Brolucizumab，新一代anti-VEGF)凭借其单链抗体超小分子结构，能更快穿透并抵达视网膜深层，实现强效控液。III期研究显示，针对nAMD，首年注射次数可降至约7次；基因治疗（ADVM022、RGX314，AAV载体）单次给药可长期抑制VEGF，Ⅰ/Ⅱ期试验显示长效控病效果。
2) 补体通路：SAR446597 (靶向C1s和B因子) 治疗因AMD导致GA的创新单次玻璃体内基因疗法于2025年7月获FDA快速通道资格，通过双靶点抑制补体经典和旁路途径，旨在实现视网膜微环境的长期补体抑制，显著降低治疗负担。
3) 多靶点协同：依莫芙普 (IBI302，抗VEGF-抗补体双靶点) 在2025年5月公布的II期研究一年数据显示，该药在治疗nAMD时，超过80%的患者在负荷期后能维持每12周的给药间隔，在视力改善上非劣效于阿柏西普，并显示出延缓黄斑萎缩发生的潜力。三优生物开发的针对AMD的三特异性抗体目前已进入临床前研发阶段。
▲ 图3：年龄相关性黄斑病变（AMD）top20靶点汇总（生物药）
02 糖尿病视网膜病变（DR）/糖尿病性黄斑水肿（DME）：糖友的“隐形视力小偷”
01
疾病分类及发病率
糖尿病视网膜病变（Diabetes retinopathy，DR）是糖尿病最常见的微血管并发症，DR按病情分非增殖期（NPDR，Ⅰ～Ⅲ期）与增殖期（PDR，Ⅳ～Ⅵ期）；糖尿病性黄斑水肿（Diabetes macular edema，DME）是DR的严重并发症，因黄斑区血管渗漏致积液，直接损害中心视力，可发生于DR各阶段。早期无症状（仅30%患者主动就医），进展至Ⅲ期以上可出现视物模糊、变形，增殖期可引发玻璃体积血、牵拉性视网膜脱离；“代谢记忆”效应显著，即使血糖控制达标，病情仍可能持续进展。
2020年全球DR患者超1.03亿，预计2045年增至1.61亿；我国糖尿病患者超1.4亿，约1/4合并DR，DME在我国视力受损人群中患病率达6.81%，是工作年龄人群视力丧失首要原因。
02
致病机制
长期高血糖触发“炎症氧化应激血管损伤”连锁反应：
a. 高血糖激活多元醇通路、PKC通路（氧化应激关键通路）、己糖胺通路，生成大量活性氧（ROS），损伤视网膜血管内皮细胞。
b. 晚期糖基化终产物（AGEs）结合受体RAGE，放大炎症反应，释放IL1β、TNFα等促炎因子，激活NFκB通路（炎症核心）。
c. VEGF过表达导致血视网膜屏障（BRB）破坏，血管渗漏与新生血管形成，同时伴随周细胞丢失、基底膜增厚。
▲ 图4：糖尿病视网膜病变（DR）的致病机制
03
已上市治疗方案与药物
针对VEGF介导的血管渗漏、炎症因子触发的血视网膜屏障破坏以及视网膜缺血等核心环节，DR/DME的临床治疗已形成了一套从基础疾病管理到靶向干预、从药物到手术的阶梯化综合策略。下表详细列出了相应的治疗方案及其作用靶点。
▼ 表3 DR/DME治疗方案与药物
04
热门在研靶点与新兴疗法
1）以VEGF为基础的多靶点抗体：Faricimab（VEGF&Ang2）拓展至DME治疗，III期研究（YOSEMITE/RHINE）pooled分析（2025年2月）显示，在100周内，相比阿柏西普，接受Faricimab治疗的患者视网膜中心凹下厚度（CST）降低更显著，无IRF（视网膜内积液）的患者比例更高，且首次达到无IRF的中位时间提早了40周；EB-105 (靶向VEGF, Ang-2, IL-6R的五价三特异性抗体) 2025年6月公布的Ib期单次剂量递增（LOTUS Part 1）研究显示，DME患者单次注射后3个月，所有剂量组均观察到BCVA（最佳矫正视力）提升和CST降低，且未出现药物相关不良事件。
2）非VEGF通路： Nintedanib (多受体酪氨酸激酶抑制剂，靶点包括VEGFR, PDGFR, FGFR等) 2025年6月的一项机制研究发现，Nintedanib能显著抑制PDR患者玻璃体液诱导的人视网膜微血管内皮细胞的Akt/Erk通路激活和管状结构形成，这为治疗抗VEGF药物疗效不佳的PDR提供了新的潜在方向。
▲ 图5：糖尿病视网膜病变（DR）top20靶点分布（生物药）
03 甲状腺相关眼病（TED）：自身免疫性眼眶“麻烦制造者”
01
疾病分类及发病率
Graves病（Graves’ Disease，GD）是最主要的甲状腺外表现，属自身免疫性眼眶疾病，因免疫系统误攻眼眶组织（成纤维细胞、前脂肪细胞），导致眼眶组织肿胀、眼球突出（突眼）、复视、视神经受压，严重时致盲。与GD高度关联（约50%GD患者继发TED），3%～5%患者出现严重病情；吸烟是重要风险因素，会加剧炎症与组织纤维化；病程分活动期（炎症活跃，适合药物干预）与稳定期（以纤维化为主，需手术矫正）。
全球TED发病率约5例/10万人/年，总体人群患病率155/100,000；我国GD患者超千万，按50%继发率估算，TED患者规模超500万。
02
致病机制
自身免疫“误判”引发的眼眶组织病理连锁反应：
a. 抗促甲状腺激素受体（TSHR）抗体攻击眼眶成纤维细胞（OFs），激活TSHR与IGF1R交叉信号。
b. OFs激活后分泌透明质酸（吸水致组织肿胀）、促炎因子（吸引T细胞、巨噬细胞浸润），同时分化为脂肪细胞与肌成纤维细胞。
c. 眼眶脂肪增多+眼外肌肿胀，导致眶内压升高，引发突眼、复视，严重时压迫视神经致损伤。
▲ 图6：甲状腺相关眼病（TED）的致病机制
03
已上市治疗方案与药物
针对甲状腺相关眼病中自身抗体触发的IGF-1R/TSHR信号通路异常、眼眶成纤维细胞活化及局部炎症反应等核心环节，其临床管理需严格依据疾病活动性与严重度进行分层，形成了从基础抗氧化到靶向抑制、从药物到手术的精准治疗路径。
▼ 表4 TED治疗方案与药物
04
热门在研靶点与新兴疗法
1）TSHR拮抗剂：新型单克隆抗体（K170TM、GenSci098）直接阻断抗TSHR抗体结合，Ⅰ/Ⅱ期试验显示突眼改善率超60%，且无IGF1R相关副作用；小分子TSHR抑制剂进入临床前研究，有望口服给药。
2）IGF-1R抑制剂（Veligrotug，VRDN-001）: 其皮下注射剂型的关键研究已完成招募，数据预计于2026年第一/二季度公布。
3）IL6受体拮抗剂（Tocilizumab）：一项针对中重度、激素耐药TED患者的研究显示，治疗16周后，93.3%的Tocilizumab组患者CAS评分较基线改善≥2分，而安慰剂组为58.8%。
4）FcRn抑制剂（Batoclimab）：2024年12月公布的中国II期研究显示，治疗第9周，1mg/kg组别的患者突眼改善应答率高达68.8%，显著优于安慰组的31.3%。同时，血清总IgG水平平均降低超过60%。
▲ 图7：甲状腺相关眼病（TED）靶点分布（生物药）
04 总结：眼科抗体药物的“破局”与“未来”
眼科抗体药物的浪潮，正以前所未有的精准度重塑着疾病的治疗格局。在AMD与DME领域，抗VEGF药物率先“破局”，成功遏制异常血管生成与渗漏，将无数患者从失明的边缘拉回，堪称视网膜疾病的里程碑。如今，这股力量正延伸至TED等自身免疫性疾病，通过靶向IGF-1R等关键通路，直击病灶背后的免疫炎症核心，为“突眼”等难题提供了全新解法。
展望未来，我们已站在“二次破局”的起点：双靶点药物、更长久的疗效、以及向更早期干预的迈进，将共同定义眼科抗体药物的新篇章。这不仅是技术的进化，更是治疗理念从“被动干预”到“主动掌控”的深刻变革。
Sanyou 10th Anniversary: A New Frontier in Ophthalmology: Targeted Antibody Therapies Illuminating the Path Forward
The eye is the most important sensory organ in the human body, responsible for perceiving over 80% of external information. Eye health is not only related to a person's quality of life but also serves as a crucial indicator of a nation's population health status. However, data from the World Health Organization (WHO) indicates that at least 2.2 billion people globally have vision impairment or blindness, of which at least 1 billion cases are preventable or treatable. The prevention and treatment of ophthalmic diseases are already urgent.
▲ Figure 1. Location and Clinical Manifestations of Common Causes of Vision Impairment
The current spectrum of ophthalmic diseases is wide. While refractive errors and conjunctivitis have a large patient base, cataracts and glaucoma are the leading causes of blindness. Retinal diseases and thyroid-associated ophthalmopathy, due to their complex mechanisms and poor prognosis, constitute the current key challenges in diagnosis and treatment. Current diagnostic and therapeutic strategies have formed a diversified system combining optical correction, surgical intervention, and drug therapy. However, with the deepening understanding of ocular immune-inflammatory mechanisms and breakthroughs in antibody drug development, the treatment model has evolved from anti-VEGF drug-led targeted therapy towards a new stage emphasizing both systemic immune regulation and local precise intervention, marking the entry of ophthalmology into an era of precision and systematization in diagnosis and treatment.
▼ Table 1 Summary of Common Ophthalmic Diseases
01 Age-Related Macular Degeneration (AMD): The "Leading Cause" of Blindness in the Elderly
01
Disease Classification and Incidence Rate
Age-related macular degeneration (AMD) is a degenerative fundus disease primarily affecting the macular region of the retina. It is divided into two main subtypes: dry (atrophic or geographic atrophy, GA), accounting for 90% of cases, and wet (neovascular, nAMD), accounting for only 10% but being the main cause of severe vision loss. Incidence increases significantly in people over 65 (reaching 10% in North America/Europe) and exceeds 36.7/1000 in those over 90. Early dry AMD is often asymptomatic; late stage causes central visual field defects due to photoreceptor cell loss. nAMD can lead to blindness in a short period due to leakage from choroidal neovascularization (CNV).
In 2020, there were 196 million AMD patients globally, projected to surge to 288 million by 2040. In the US, there were already 20 million patients in 2019, of which 1.5 million were advanced severe cases. Prevalence is significantly higher in Europeans (12.33%) compared to Asians (7.38%) and Africans (7.53%).
02
Pathogenic Mechanisms
a. Dry AMD: Chronic low-grade inflammation + overactivation of the complement system lead to subretinal drusen, subretinal drusenoid deposits (SDD), progressively causing retinal pigment epithelium (RPE) cell and photoreceptor degeneration and atrophy.
b. Wet AMD: Inflammation, hypoxia, etc., trigger angiogenesis. Mast cells and macrophages release vascular endothelial growth factor (VEGF), disrupting the VEGF/pigment epithelium-derived factor (PEDF) balance. Abnormal CNV breaks through Bruch's membrane, causing leakage, hemorrhage, and scarring.
▲ Figure 2: Pathogenesis of Age-Related Macular Degeneration (AMD)
03
Marketed Treatment Options and Drugs
In-depth understanding of these key pathological mechanisms has directly driven the development of targeted therapeutic drugs. Current treatment strategies focus on precisely intervening in the above pathways: inhibiting VEGF to control abnormal blood vessel growth in wet AMD, or modulating the complement pathway to delay the progression of dry AMD. Representative marketed drugs are listed below:
▼ Table 2 AMD Treatment Options and Drugs
04
Popular Targets Under Research and Emerging Therapies
1) VEGF Pathway: Brolucizumab (a new generation anti-VEGF), with its single-chain antibody ultra-small molecular structure, penetrates faster and reaches deeper retinal layers, achieving potent fluid control. Phase III studies showed that for nAMD, the number of injections in the first year could be reduced to about 7. Gene therapies (ADVM022, RGX314, AAV vector) offer long-term VEGF suppression with a single administration; Phase I/II trials show long-lasting disease control effects.
2) Complement Pathway: SAR446597 (targeting C1s and Factor B), an innovative single-intravitreal gene therapy for GA due to AMD, received FDA Fast Track designation in July 2025. By dually inhibiting the classical and alternative complement pathways, it aims to achieve long-term complement suppression in the retinal microenvironment, significantly reducing treatment burden.
3) Multi-Target Synergy: IBI302 (anti-VEGF & anti-complement dual-target) in one-year Phase II data announced in May 2025 showed that over 80% of nAMD patients maintained a 12-week dosing interval after the loading phase, demonstrating non-inferior visual acuity improvement compared to Aflibercept, and showing potential to delay macular atrophy. A trispecific antibody developed by Sanyou Bio has currently entered the preclinical research stage.
▲ Figure 3: Summary of Top 20 Targets for Age-Related Macular Degeneration (AMD) (Biologics)
02 Diabetic Retinopathy (DR) / Diabetic Macular Edema (DME): The "Invisible Vision Thief" for Diabetics
01
Disease Classification and Incidence Rate
Diabetic retinopathy (DR) is the most common microvascular complication of diabetes. DR is classified by severity into non-proliferative (NPDR, stages I-III) and proliferative (PDR, stages IV-VI). Diabetic macular edema (DME) is a serious complication of DR, where fluid leakage from blood vessels in the macula causes fluid accumulation, directly impairing central vision, and can occur at any stage of DR. Early stages are asymptomatic (only 30% of patients seek medical attention proactively). Progressing to stage III and above can cause blurred or distorted vision. The proliferative stage can lead to vitreous hemorrhage and tractional retinal detachment. The "metabolic memory" effect is significant; even after achieving glycemic control, the condition may continue to progress.
In 2020, there were over 103 million DR patients globally, projected to increase to 161 million by 2045. China has over 140 million diabetics, about one-quarter of whom develop DR. DME prevalence in China's vision-impaired population reaches 6.81%, making it the leading cause of vision loss in the working-age population.
02
Pathogenic Mechanisms
Long-term hyperglycemia triggers a chain reaction of "inflammatory oxidative stress vascular injury":
a. Hyperglycemia activates the polyol pathway, PKC pathway (a key oxidative stress pathway), and hexosamine pathway, generating large amounts of reactive oxygen species (ROS), damaging retinal vascular endothelial cells.
b. Advanced glycation end products (AGEs) bind to the receptor RAGE, amplifying the inflammatory response, releasing pro-inflammatory cytokines like IL-1β, TNF-α, and activating the NF-κB pathway (core of inflammation).
c. VEGF overexpression leads to breakdown of the blood-retinal barrier (BRB), vascular leakage and neovascularization, accompanied by pericyte loss and basement membrane thickening.
▲ Figure 4: Pathogenic Mechanisms of Diabetic Retinopathy (DR)
03
Marketed Treatment Options and Drugs
Targeting core aspects such as VEGF-mediated vascular leakage, cytokine-triggered BRB disruption, and retinal ischemia, clinical management of DR/DME has formed a tiered comprehensive strategy ranging from basic disease management to targeted intervention, and from drugs to surgery. The table below details the corresponding treatment options and their targets.
▼ Table 3 DR/DME Treatment Options and Drugs
04
Popular Targets Under Research and Emerging Therapies
1) VEGF-based Multi-Target Antibodies: Faricimab (VEGF & Ang2) extended to DME treatment. A pooled analysis of Phase III studies (YOSEMITE/RHINE) in February 2025 showed that over 100 weeks, compared to Aflibercept, Faricimab-treated patients had significantly greater reduction in central subfield thickness (CST), a higher proportion of patients were free of intraretinal fluid (IRF), and the median time to first achieve IRF-free status was 40 weeks earlier. EB-105 (a pentavent trispecific antibody targeting VEGF, Ang-2, IL-6R): Ib phase single-dose escalation (LOTUS Part 1) study results announced in June 2025 showed that 3 months after a single injection in DME patients, all dose groups observed improvements in BCVA and reductions in CST, with no drug-related adverse events reported.
2) Non-VEGF Pathways: Nintedanib (a multi-receptor tyrosine kinase inhibitor targeting VEGFR, PDGFR, FGFR, etc.): A mechanistic study in June 2025 found that Nintedanib significantly inhibited Akt/Erk pathway activation and tube formation induced by vitreous fluid from PDR patients in human retinal microvascular endothelial cells, providing a new potential direction for treating PDR patients with poor response to anti-VEGF drugs.
▲ Figure 5: Distribution of Top 20 Targets for Diabetic Retinopathy (DR) (Biologics)
03 Thyroid Eye Disease (TED): The Autoimmune Orbital "Troublemaker"
01
Disease Classification and Incidence Rate
Graves' orbitopathy (GO) or Thyroid Eye Disease (TED) is the primary extra-thyroidal manifestation of Graves' Disease (GD), an autoimmune orbital disease. It occurs when the immune system mistakenly attacks orbital tissues (fibroblasts, preadipocytes), leading to orbital tissue swelling, exophthalmos (protruding eyes), diplopia (double vision), and optic nerve compression, potentially causing blindness in severe cases. Highly associated with GD (about 50% of GD patients develop TED), with 3%-5% of patients experiencing severe disease. Smoking is a significant risk factor, exacerbating inflammation and tissue fibrosis. The disease course is divided into an active phase (active inflammation, suitable for drug intervention) and a stable phase (dominated by fibrosis, requiring surgical correction).
The global incidence of TED is approximately 5 cases per 100,000 people per year, with an overall population prevalence of 155/100,000. China has over 10 million GD patients; estimating a 50% complication rate, the TED patient population exceeds 5 million.
02
Pathogenic Mechanisms
A pathological chain reaction in orbital tissues triggered by autoimmune "misdirection":
a. Anti-thyrotropin receptor (TSHR) antibodies attack orbital fibroblasts (OFs), activating cross-signaling between TSHR and IGF-1R.
b. Activated OFs secrete hyaluronic acid (absorbing water causing tissue swelling) and pro-inflammatory cytokines (attracting T cells, macrophages), while differentiating into adipocytes and myofibroblasts.
c. Increased orbital fat + swollen extraocular muscles lead to elevated intraorbital pressure, causing exophthalmos, diplopia, and in severe cases, compressing and damaging the optic nerve.
▲ Figure 6: Pathogenesis of Thyroid Eye Disease (TED)
03
Marketed Treatment Options and Drugs
Targeting the core aspects of TED—autoantibody-triggered IGF-1R/TSHR signaling pathway abnormalities, orbital fibroblast activation, and local inflammatory responses—clinical management requires strict stratification based on disease activity and severity, forming a precise treatment pathway from basic antioxidant therapy to targeted inhibition, and from drugs to surgery.
▼ Table 4 TED Treatment Options and Drugs
04
Popular Targets Under Research and Emerging Therapies
1) TSHR Antagonists: Novel monoclonal antibodies (K1-70™, GenSci098) directly block anti-TSHR antibody binding. Phase I/II trials show exophthalmos improvement rates over 60%, without IGF-1R related side effects. Small molecule TSHR inhibitors are in preclinical research, potentially offering oral administration.
2) IGF-1R Inhibitors (Veligrotug, VRDN-001): The key study for its subcutaneous formulation has completed enrollment, with data expected in Q1/Q2 2026.
3) IL-6 Receptor Antagonist (Tocilizumab): A study in patients with moderate-to-severe, steroid-resistant TED showed that after 16 weeks of treatment, 93.3% of the Tocilizumab group had a CAS score improvement ≥2 points from baseline, compared to 58.8% in the placebo group.
4) FcRn Inhibitor (Batoclimab): Chinese Phase II results announced in December 2024 showed that at week 9, the response rate for exophthalmos improvement in the 1mg/kg group was 68.8%, significantly higher than the 31.3% in the placebo group. Simultaneously, serum total IgG levels were reduced by over 60% on average.
▲ Figure 7: Target Distribution for Thyroid Eye Disease (TED) (Biologics)
04 Conclusion: The "Breakthrough" and "Future" of Ophthalmic Antibody Drugs
The wave of ophthalmic antibody drugs is reshaping the treatment landscape for diseases with unprecedented precision. In the fields of AMD and DME, anti-VEGF drugs led the initial "breakthrough," successfully curbing abnormal angiogenesis and leakage, pulling countless patients back from the brink of blindness—a true milestone for retinal diseases. Now, this force is extending to autoimmune diseases like TED, targeting key pathways such as IGF-1R to directly address the core immune-inflammatory drivers behind conditions like "exophthalmos," offering new solutions.
Looking ahead, we stand at the starting point of a "second breakthrough": dual-target drugs, longer-lasting efficacy, and moving towards earlier intervention will collectively define the new chapter for ophthalmic antibody drugs. This is not just a technological evolution but a profound shift in treatment philosophy from "passive intervention" to "active control."
▶ References
Burton MJ, Ramke J, Marques AP, et al. (2021). The Lancet Global Health Commission on Global Eye Health: vision beyond 2020. The Lancet. Global health, 9(4), e489–e551.
ElSheikh R H, Chauhan M Z, Sallam A B. Current and novel therapeutic approaches for treatment of neovascular age-related macular degeneration[J]. Biomolecules, 2022, 12(11): 1629
Han, H., Li, S., Xu, M., Zhong, Y., Fan, W., Xu, J., Zhou, T., Ji, J., Ye, J., & Yao, K. (2023). Polymer- and lipid-based nanocarriers for ocular drug delivery: Current status and future perspectives. Advanced drug delivery reviews, 196, 114770.
Gulbins, A., Görtz, G. E., Gulbins, E., & Eckstein, A. (2023). Sphingolipids in thyroid eye disease. Frontiers in endocrinology, 14, 1170884.
Fleckenstein, M., Schmitz-Valckenberg, S., & Chakravarthy, U. (2024). Age-Related Macular Degeneration: A Review. JAMA, 331(2), 147–157.
Wiersinga, W. M., Eckstein, A. K., & Žarković, M. (2025). Thyroid eye disease (Graves' orbitopathy): clinical presentation, epidemiology, pathogenesis, and management. The lancet. Diabetes & endocrinology, 13(7), 600–614.
Tang, L., Xu, G. T., & Zhang, J. F. (2023). Inflammation in diabetic retinopathy: possible roles in pathogenesis and potential implications for therapy.
Seo, H., Park, S. J., & Song, M. (2025). Diabetic Retinopathy (DR): Mechanisms, Current Therapies, and Emerging Strategies. Cells, 14(5), 376.
Tan, T. E., & Wong, T. Y. (2023). Diabetic retinopathy: Looking forward to 2030. Frontiers in endocrinology, 13, 1077669.
Thomas,C. N., Sim, D. A., Lee, W. H., Alfahad, N., Dick, A. D., Denniston, A. K., & Hill, L. J. (2022). Emerging therapies and their delivery for treating age-related macular degeneration. British journal of pharmacology, 179(9), 1908–1937.
Qu,S., Lin, H., Pfeiffer, N., & Grus, F. H. (2024). Age Related Macular Degeneration and Mitochondria-Associated Autoantibodies: A Review of the Specific Pathogenesis and Therapeutic Strategies. International journal of molecular sciences, 25(3), 1624.
Wong, T. Y., Cheung, C. M., Larsen, M., Sharma, S., & Simó, R. (2016). Diabetic retinopathy. Nature reviews. Disease primers, 2, 16012.
Sivaprasad, S., Wong, T. Y., Gardner, T. W., Sun, J. K., & Bressler, N. M. (2025). Diabetic retinal disease. Nature reviews. Disease primers, 11(1), 62.
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