Current uses of ophthalmic lasers.

Current laser treatments are quick, relatively painless, and well tolerated. Some ophthalmic techniques can be performed only by laser while others have a lower morbidity than alternative treatments. Peripheral retinal photocoagulation and focal photocoagulation now offer greatly improved visual prognosis for diabetic patients with proliferative diabetic retinopathy or diabetic macular disease. Selected cases of macular degeneration may be treated by focal laser photocoagulation. The role of lasers in treating sub-retinal neovascular membranes is limited by the extent and location of the membrane at presentation and the high risk of recurrence after treatment. Patients with distorted vision must be referred urgently for specialist ophthalmic assessment. Flat retinal holes and tears may be sealed by laser therapy, thus preventing retinal detachment. Short pulsed neodymium-YAG photodisruptive capsulotomy effectively clears the visual axis of thickened posterior lens capsule after cataract surgery. Short pulsed neodymium-YAG photodisruptive iridotomy may be used to treat and prevent angle closure glaucoma. Laser trabeculoplasty aids the control of open angle glaucoma. Research is continuing into the role of other lasers in managing open angle glaucoma and of photoablative lasers in treating refractive errors and superficial corneal disorders.     

Retinal cross-section motion correction in three-dimensional retinal optical coherence tomography

Motion correction is an important issue in ophthalmic optical coherence tomography (OCT), and can improve the ability of data sets to reflect the physiological structures of tissues and make visualization and subsequent analysis easier. In this study, we present a novel method to correct the cross-sectional motion artifacts in retinal OCT volumes. Motion along the x-direction (fast-scan direction) is corrected through the normalized cross-correlation algorithm, while axial motion compensation is performed using the polynomial fitting method on the inner segment/outer segment (IS/OS) layer segmented by the shortest path faster algorithm (SPFA). The results of volunteers with central serous chorioretinopathy demonstrate that the proposed method effectively corrects motion artifacts in OCT volumes and may have potential application value in the evaluation of ophthalmic diseases such as diabetic retinopathy, glaucoma and age-related macular degeneration.     

Relationship Between the Environmental Endocrine Disruptor Bisphenol a and Dyslipidemia: A Five-Year Prospective Study

Objective: To investigate whether serum bisphenol A (BPA) concentration is related to the occurrence of dyslipidemia.Methods: A total of 574 adults were enrolled at baseline and followed up for 5 years. Concentrations of serum BPA, triglycerides (TGs), low-density lipoprotein (LDL) cholesterol, and high-density lipoprotein (HDL) cholesterol were measured. Dyslipidemia was defined as the existence of one or more of the following conditions: high-LDL-cholesterolemia (LDL ≥140 mg/dL), hypertriglyceridemia (TGs ≥150 mg/dL), or low-HDL-cholesterolemia (HDL <40 mg/dL). Participants were stratified into tertiles according to low, median, and high baseline serum BPA levels. Multivariable linear and logistic regression models were used. Data from baseline and follow-up were used for cross-sectional and longitudinal analyses, respectively.Results: In the cross-sectional analysis, compared to subjects in the low BPA tertile, those in the high BPA tertile showed a higher level of LDL cholesterol (108.1 ± 24.4 mg/dL versus 119.5 ± 26.9 mg/dL; P<.05) and a lower level of HDL cholesterol (46.2 ± 11.7 mg/dL versus 39.5 ± 7.5 mg/dL; P<.05). In multivariable linear regression models, Z-transformed BPA was positively associated with LDL cholesterol (β= 0.13, P = .002) and negatively associated with HDL cholesterol (β= -0.28; P<.001). After cross-sectionally adjusting for confounders, subjects in higher BPA exposure was associated with a higher prevalence of low-HDL-cholesterolemia. Longitudinally, in subjects without low-HDL-cholesterolemia at baseline, each SD increment in baseline BPA was associated with a higher incidence of low-HDL-cholesterolemia after adjustment for confounders (odds ratio [95% confidence interval; CI] 2.76, 95% CI 1.21, 6.29).Conclusion: Cross-sectionally, higher BPA exposure is associated with a higher prevalence of low-HDL-cholesterolemia. Longitudinally, baseline BPA is an independent predictor of the 5-year incidence of low-HDL-cholesterolemia.Abbreviations: BMI = body mass index; BPA = bisphenol A; CI = confidence interval; CVD = cardiovascular disease; EIMDS = environment, inflammation and metabolic diseases study; HDL = high density lipoprotein; LDL = low density lipoprotein; OR = odds ratio; PPAR = peroxisome proliferator-activated receptor; SBP = systolic blood pressure; TG = triglyceride; Z-BPA = Z-transformed bisphenol A     

Prevalence and associated factors of dyslipidemia in the adult Chinese population

To determine the prevalence, associated factors, awareness and control of dyslipidemia in Chinese living in Greater Beijing, we measured the serum cholesterol concentration in 3251 Chinese adults (age: 45 to 89 years) as participants of the population-based Beijing Eye Study 2006. Additional information on treatment of dyslipidemia was obtained using a standard questionnaire. The mean concentrations of total, HDL cholesterol, LDL cholesterol and triglycerides were 4.92±1.01 mmol/L, 1.61±0.36 mmol/L, 2.88±0.85 mmol/L, and 1.76±1.29 mmol/L, respectively. Prevalence of dyslipidemia was 56.1±0.9%%. Presence of dyslipidemia was significantly associated with increasing age (odds ratio (OR):1.02; 95% confidence interval (CI): 1.01, 1.03), female gender (OR:1.51; 95%CI: 1.25, 1.83), urban region (OR:1.82; 95%CI: 1.30, 2.55), body mass index (OR:1.13; 95%CI: 1.10, 1.15), income (OR:1.11; 95%CI:1.02, 1.21), blood glucose concentration (OR:1.10; 95%CI:1.05, 1.16), diastolic blood pressure (OR:1.02; 95%CI: 1.01, 1.03), and smoking (OR:1.23; 1.01, 1.51). Among those who had dyslipidemia, the proportion of subjects who were aware, treated and controlled was 50.9%, 23.8%, and 39.91%, respectively. The awareness rate was associated with urban region (P = 0.001; OR: 6.50), body mass index (P = 0.001; OR:1.06), and income (P = 0.02; OR:1.14). The data suggest that dyslipidemia may be present in about 56% of the population aged 45+ years in Greater Beijing. Factors likely associated with dyslipidemia were higher age, female gender, urban region, higher body mass index, higher income, higher blood concentration of glucose, higher diastolic blood pressure, and smoking. In the examined study population, treatment rate was 24% with about 60% of the treated subjects still having uncontrolled dyslipidemia.     

Age-Related Vitamin D Deficiency Is Associated with Reduced Macular Ganglion Cell Complex: A Cross-Sectional High-Definition Optical Coherence Tomography Study

Background

Vitamin D deficiency is associated with smaller volume of optic chiasm in older adults, indicating a possible loss of the visual axons and their cellular bodies. Our objective was to determine whether vitamin D deficiency in older adults is associated with reduced thickness of the ganglion cell complex(GCC) and of the retinal nerve fibre layer(RNFL), as measured with high-definition optical coherence tomography(HD-OCT).

Methods

Eighty-five French older community-dwellers without open-angle glaucoma and patent age-related macular degeneration(mean, 71.1±4.7years; 45.9%female) from the GAIT study were separated into 2 groups according to serum 25OHD level(i.e., deficient≤25nmol/L or sufficient>25nmol/L). Measurements of GCC and RNFL thickness were performed using HD-OCT. Age, gender, body mass index, number of comorbidities, dementia, functional autonomy, intracranial volume, visual acuity, serum calcium concentration and season of testing were considered as potential confounders.

Results

Mean serum 25OHD concentration was 58.4±26.8nmol/L. Mean logMAR visual acuity was 0.03±0.06. Mean visual field mean deviation was -1.25±2.29dB. Patients with vitamin D deficiency(n=11) had a reduced mean GCC thickness compared to those without vitamin D deficiency(72.1±7.4μm versus 77.5±7.5μm, P=0.028). There was no difference of the mean RNFL thickness in these two groups(P=0.133). After adjustment for potential confounders, vitamin D deficiency was associated with reduced GCC thickness(ß=-5.12, P=0.048) but not RNFL thickness(ß=-9.98, P=0.061). Specifically, vitamin D deficiency correlated with the superior medial GCC area(P=0.017) and superior temporal GCC area(P=0.010).

Conclusions

Vitamin D deficiency in older patients is associated with reduced mean GCC thickness, which can represent an early stage of optic nerve damage, prior to RNFL loss.     

雷珠单抗与阿柏西普玻璃体腔注射治疗渗出性年龄相关性黄斑变性的疗效观察

目的:探究雷珠单抗与阿柏西普玻璃体腔注射治疗渗出性年龄相关性黄斑变性的临床疗效与安全性。方法:选取2015年5月～2018年5月我院收治的渗出性年龄相关性黄斑变性患者98例(98眼),采用随机数字表法将患者分为两组,A组玻璃体腔内缓慢注射0.05 m L(0.5 mg)雷珠单抗注射液,B组玻璃体腔内缓慢注射0.05 m L(2 mg)阿柏西普注射液。比较两组患者的视力改善情况、眼动脉血流动力学、黄斑中心凹视网膜厚度及不良反应的发生情况。结果:治疗前两组患者的视力比较无统计学差异(P0.05),治疗后,B组视力显著高于A组(P0.05);。两组患者治疗前后眼动脉血流动力学相关指标比较均无统计学差异(P0.05)。;两组患者治疗后的黄斑中心凹视网膜厚度均显著降低,且治疗3个月B组治疗3个月显著低于A组(P0.05);B组患者注射药物后结膜下大出血发生率显著低于A组(P0.05)。结论:阿柏西普可显著改善渗出性年龄相关性黄斑变性患者的视力,且安全性高,可能与其可显著改善患者的黄斑中心凹视网膜厚度有关,且不良反应发生率低,安全性好。     

Metformin and retinal diseases in preclinical and clinical studies: Insights and review of literature

Metformin is one of the most prescribed drugs in the world giving potential health benefits beyond that of type 2 diabetes (T2DM). Emerging evidence suggests that it may have protective effects for retinal/posterior segment diseases including diabetic retinopathy (DR), age-related macular degeneration (AMD), inherited retinal degeneration such as retinitis pigmentosa (RP), primary open angle glaucoma (POAG), retinal vein occlusion (RVO), and uveitis. Metformin exerts potent anti-inflammatory, antiangiogenic, and antioxidative effects on the retina in response to pathologic stressors. In this review, we highlight the broad mechanism of action of metformin through key preclinical studies on animal models and cell lines used to simulate human retinal disease. We then explore the sparse but promising retrospective clinical data on metformin’s potential protective role in DR, AMD, POAG, and uveitis. Prospective clinical data is needed to clarify metformin’s role in management of posterior segment disorders. However, given metformin’s proven broad biochemical effects, favorable safety profile, relatively low cost, and promising data to date, it may represent a new therapeutic preventive and strategy for retinal diseases.     

Fas ligand (CD95 ligand) controls angiogenesis beneath the retina

A principal cause of blindness is subretinal neovascularization associated with age-related macular degeneration. Excised neovascular membranes from patients with age-related macular degeneration demonstrated a pattern of Fas+ new vessels in the center of the vascular complex, surrounded by FasL+ retinal pigment epithelial cells. In a murine model, Fas (CD95)-deficient (Ipr) and FasL-defective (gld) mice had a significantly increased incidence of neovascularization compared with normal mice. Furthermore, in gld mice there is massive subretinal neovascularization with uncontrolled growth of vessels. We found that cultured choroidal endothelial cells were induced to undergo apoptosis by retinal pigment epithelial cells through a Fas-FasL interaction. In addition, antibody against Fas prevented vascular tube formation of choroidal endothelial cells derived from the eye in a three-dimensional in vitro assay. Thus, FasL expressed on retinal pigment epithelial cells may control the growth and development of new subretinal vessels that can damage vision.     

Association between Blood Lead Levels and Age-Related Macular Degeneration

Purpose

To investigate the association between blood lead levels and prevalence of age-related macular degeneration (AMD).

Methods

A nationwide population-based cross-sectional study included 4,933 subjects aged over 40 years who participated in the 2008–2012 Korean National Health and Nutrition Examination Survey, and for whom fundus photographs were available. All participants underwent a standardized interview, evaluation of blood lead concentration, and a comprehensive ophthalmic examination. Digital fundus photographs (45°) were taken of both eyes under physiological mydriasis. All fundus photographs were graded using an international classification and grading system.

Results

Mean blood lead levels were 3.15 μg/dL in men and 2.27 μg/dL in women (P < 0.001). After adjusting for potential confounders including age, gender, smoking status, total cholesterol levels, triglyceride levels, heart problems and strokes, the adjusted odds ratio (OR) in women for any AMD was 1.86 (95% Confidence Interval [CI], 1.03–3.36) and for early AMD was 1.92 (95% CI, 1.06–3.48), for those in the highest quintile of lead level compared with the lowest quintile. In men, however, blood lead level was not significantly associated with AMD.

Conclusions

Blood lead levels were higher in men, but were only associated with AMD in women. Increased levels of blood lead may be involved in the pathogenesis of AMD development in women.     

Retinal cone and rod photoreceptor cells exhibit differential susceptibility to light-induced damage

All-trans-retinal and its condensation-products can cause retinal degeneration in a light-dependent manner and contribute to the pathogenesis of human macular diseases such as Stargardt's disease and age-related macular degeneration. Although these toxic retinoid by-products originate from rod and cone photoreceptor cells, the contribution of each cell type to light-induced retinal degeneration is unknown. In this study, the primary objective was to learn whether rods or cones are more susceptible to light-induced, all-trans-retinal-mediated damage. Previously, we reported that mice lacking enzymes that clear all-trans-retinal from the retina, ATP-binding cassette transporter 4 and retinol dehydrogenase 8, manifested light-induced retinal dystrophy. We first examined early-stage age-related macular degeneration patients and found retinal degenerative changes in rod-rich rather than cone-rich regions of the macula. We then evaluated transgenic mice with rod-only and cone-like-only retinas in addition to progenies of such mice inbred with Rdh8(-/-) Abca4(-/-) mice. Of all these strains, Rdh8(-/-) Abca4(-/-) mice with a mixed rod-cone population showed the most severe retinal degeneration under regular cyclic light conditions. Intense light exposure induced acute retinal damage in Rdh8(-/-) Abca4(-/-) and rod-only mice but not cone-like-only mice. These findings suggest that progression of retinal degeneration in Rdh8(-/-) Abca4(-/-) mice is affected by differential vulnerability of rods and cones to light.     

Y402H polymorphism of complement factor H affects binding affinity to C-reactive protein

Complement factor H (FH) is an important regulator of the alternative complement pathway. The Y402H polymorphism within the seventh short consensus repeat of FH was recently shown to be associated with age-related macular degeneration, the most common cause of irreversible blindness in the Western world. We examined the effects of this polymorphism on various FH functions. FH purified from sera of age-related macular degeneration patients homozygous for the FH(402H) variant showed a significantly reduced binding to C-reactive protein (CRP), an acute phase protein, as compared with FH derived from unaffected controls homozygous for the FH(402Y) variant. Strongly reduced binding to CRP was also observed with a recombinant fragment of FH (short consensus repeat 5-7) containing the same amino acid change. Because the interaction of CRP and FH promotes complement-mediated clearance of cellular debris in a noninflammatory fashion, we propose that the reduced binding of FH(402H) to CRP could lead to an impaired targeting of FH to cellular debris and a reduction in debris clearance and enhanced inflammation along the macular retinal pigmented epithelium-choroid interface in individuals with age-related macular degeneration.     

DNA损伤与眼病相关性的研究进展

DNA损伤是复制过程中发生的DNA核苷酸序列永久性改变,并导致遗传特征改变的现象。对DNA损伤与修复的研究是现代分子生物学研究的热点之一。目前,DNA损伤对眼组织细胞凋亡、基因改变、细胞活性的影响已成为眼科疾病研究的热点。在年龄相关性白内障、老年性黄斑病变等眼科疾病的病因研究中证实氧化应激是其主要致病因素,当机体遭受有害刺激导致氧化应激时,机体、组织、细胞受到一系列损伤,而DNA的损伤对氧化应激最为敏感。本文就DNA损伤及其与晶状体上皮细胞及视网膜色素上皮细胞相关性的研究进展作一综述,为眼科疾病的研究以及防治提供新的方法及思路。     

Epidemiological aspects of ageing.

A major societal challenge is to improve quality of life and prevent or reduce disability and dependency in an ageing population. Increasing age is associated with increasing risk of disability and loss of independence, due to functional impairments such as loss of mobility, hearing and vision; a major issue must be how far disability can be prevented. Ageing is associated with loss of bone tissue, reduction in muscle mass, reduced respiratory function, decline in cognitive function, rise in blood pressure and macular degeneration which predispose to disabling conditions such as osteoporosis, heart disease, dementia and blindness. However, there are considerable variations in different communities in terms of the rate of age-related decline. Large geographic and secular variations in the age-adjusted incidence of major chronic diseases such as stroke, hip fracture, coronary heart disease, cancer, visual loss from cataract, glaucoma and macular degeneration suggest strong environmental determinants in diet, physical activity and smoking habit. The evidence suggests that a substantial proportion of chronic disabling conditions associated with ageing are preventable, or at least postponable and not an inevitable accompaniment of growing old. Postponement or prevention of these conditions may not only increase longevity, but, more importantly, reduce the period of illnesses such that the majority of older persons may live high-quality lives, free of disability, until very shortly before death. We need to understand better the factors influencing the onset of age-related disability in the population, so that we have appropriate strategies to maintain optimal health in an ageing population.     

Effects of lighting environment on the degeneration of retinal ganglion cells in glutamate/aspartate transporter deficient mice,a mouse model of normal tension glaucoma

Lighting conditions may affect the development of retinal degenerative diseases such as macular degeneration. In this study, to determine whether the lighting environment affects the progression of degeneration of retinal ganglion cells (RGCs), we examined glutamate/aspartate transporter (GLAST) heterozygous (GLAST^+/-) mice, a mouse model of normal tension glaucoma. GLAST^+/- mice were reared under a 12-h light-dark cycle (Light/Dark) or complete darkness (Dark/Dark) condition after birth. The total RGC number in the Dark/Dark group was significantly decreased compared with the Light/Dark group at 3 weeks old, while the number of osteopontin-positive αRGCs were similar in both groups. At 6 and 12 weeks old, the total RGC number were not significantly different in both conditions. In addition, the retinal function examined by multifocal electroretinogram were similar at 12 weeks old. These results suggest that lighting conditions may regulate the progression of RGC degeneration in some types of glaucoma.     

Hydroxytyrosol protects retinal pigment epithelial cells from acrolein-induced oxidative stress and mitochondrial dysfunction

Hydroxytyrosol (HTS) is a natural polyphenol abundant in olive oil. Increasing evidence indicates HTS has beneficial effect on human health for preventing various diseases. In the present study, we investigated the protective effects of HTS on acrolein-induced toxicity in human retinal pigment epithelial cell line, ARPE-19, a cellular model of smoking- and age-related macular degeneration. Acrolein, a major component of the gas phase cigarette smoke and also a product of lipid peroxidation in vivo , at 75 μmol/L for 24 h caused significant loss of cell viability, oxidative damage (increase in oxidant generation and oxidative damage to proteins and DNA, decrease in antioxidants and antioxidant enzymes, and also inactivation of the Keap1/Nrf2 pathway), and mitochondrial dysfunction (decrease in membrane potential, activities of mitochondrial complexes, viable mitochondria, oxygen consumption, and factors for mitochondrial biogenesis, and increase in calcium). Pre-treatment with HTS dose dependently and also time dependently protected the ARPE-19 cells from acrolein-induced oxidative damage and mitochondrial dysfunction. A short-term pre-treatment with HTS (48 h) required > 75 μmol/L for showing protection while a long-term pre-treatment (7 days) showed protective effect from 5 μmol/L on. The protective effect of HTS in this model was as potent as that of established mitochondria-targeting antioxidant nutrients. These results suggest that HTS is also a mitochondrial-targeting antioxidant nutrient and that dietary administration of HTS may be an effective measure in reducing and or preventing cigarette smoke-induced or age-related retinal pigment epithelial degeneration, such as age-associated macular degeneration.     

Deciphering primate retinal aging at single-cell resolution

Dear Editor, The retina is a light-sensitive highly-organized tissue,which is vulnerable to aging and age-related retinal diseases.Specifically,progressive retinal degeneration leads to visual function deterioration and vision impairment in the elderly(Lin et al.,2016).In diseases such as age-related macular degeneration(AMD),retinitis pigmentosa(RP)and diabetic retinopathy(DR),pathological process lacking effective treatments profoundly and negatively impact on the quality of life in the elderly(Lin et al.,2016;Chen et al.,2019).Thus,an in-depth molecular assessment of the mechanisms driv-ing retinal aging is of urgent scientific and medical importance.     

Mechanistically linking age-related diseases and dietary carbohydrate via autophagy and the ubiquitin proteolytic systems

Epidemiological data indicate that consuming diets that deliver sugar to the blood rapidly (called high glycemic index, GI) is associated with enhanced risk for age-related diseases such as cardiovascular disease, type 2 diabetes, cataract and age-related macular degeneration (AMD). These debilities are associated with accumulation of toxic protein aggregates as observed in other protein precipitation or amyloid diseases including Alzheimer, Parkinson and Huntington diseases and encephalopathies. Barriers to recommending lower-GI diets to promote health include the absence of established intracellular biochemical mechanisms that link high-GI diets to compromised homeostasis. The data herein corroborate the epidemiological findings and provide platforms to elucidate additional mechanistic aspects of salutary effects of consuming diets of different GIs. They are also useful for testing drugs, including autophagy enhancers, glycemia regulators, or nutraceuticals, which can be exploited to extend health.     

Mechanistically linking age-related diseases and dietary carbohydrate via autophagy and the ubiquitin proteolytic systems

Epidemiological data indicate that consuming diets that deliver sugar to the blood rapidly (called high glycemic index, GI) is associated with enhanced risk for age-related diseases such as cardiovascular disease, type 2 diabetes, cataract and age-related macular degeneration (AMD). These debilities are associated with accumulation of toxic protein aggregates as observed in other protein precipitation or amyloid diseases including Alzheimer, Parkinson and Huntington diseases and encephalopathies. Barriers to recommending lower-GI diets to promote health include the absence of established intracellular biochemical mechanisms that link high-GI diets to compromised homeostasis. The data herein corroborate the epidemiological findings and provide platforms to elucidate additional mechanistic aspects of salutary effects of consuming diets of different GIs. They are also useful for testing drugs, including autophagy enhancers, glycemia regulators, or nutraceuticals, which can be exploited to extend health.     

Alterations in liver, muscle, and adipose tissue insulin sensitivity in men with HIV infection and dyslipidemia

Dyslipidemia is common in patients with HIV infection. In this study, a two-stage euglycemic hyperinsulinemic clamp, with infusion of stable isotopically labeled tracers, was used to evaluate insulin action in skeletal muscle, liver, and adipose tissue in HIV-infected men with dyslipidemia (HIV-DL; plasma triglyceride >250 mg/dl and HDL <45 mg/dl; n=12), HIV-infected men without dyslipidemia (HIV w/o DL; n=12), and healthy men (n=6). Basal rates of glucose production (glucose R(a)), glucose disposal (glucose R(d)), and lipolysis (palmitate R(a)) were similar between groups. The relative suppression of glucose R(a) (63+/- 4, 77+/- 2, and 78+/- 3%, P=0.008) and palmitate R(a) (49+/-4, 63+/-3, and 68+/-3%, P=0.005) during ow-dose insulin infusion (plasma insulin approximately 30 microU/ml), and the relative stimulation of glucose R(d) (214+/-21, 390+/-25, and 393+/-46%, P=0.001) during high-dose insulin infusion (plasma insulin approximately 75 microU/ml) were lower in HIV-DL than in HIV w/o DL and healthy volunteers, respectively. Suppression of basal glucose R(a) correlated with plasma adiponectin (r=0.44, P=0.02) and inversely with plasma IL-6 (r=-0.49, P<0.001). Stimulation of glucose R(d) correlated directly with adiponectin (r=0.48, P<0.01) and inversely with IL-6 (r=-0.49, P=0.02). We conclude that dyslipidemia in HIV-infected men is indicative of multiorgan insulin resistance, and circulating adipokines may be important in the pathogenesis of impaired insulin action.     

Curcumin: A new candidate for retinal disease therapy?

The retina is the neural portion and light-sensitive layer of the eye, which has been observed in most of the vertebrates. The retina is composed of light-sensitive cells that absorb light and convert it into neural signals. These signals are sent to the brain for visual recognition. It has been shown that many pathogenesis conditions, including inflammation, angiogenesis, oxidative stress, and imbalanced histone modifications in the retina are associated with initiation and progression of retinal diseases (ie, glaucoma, diabetic retinopathy, and age-related macular degeneration). Currently available treatments include laser surgery, freezing, stem-cell therapy, shrinking abnormal blood vessels. It has some limitations, such as invasive methods, high costs, and many side effects. Hence, finding a new therapeutic platform for stopping or slowing of the disease progression is required. Curcumin is a natural product, which is associated with a wide range of properties, such as antioxidant, anti-inflammatory, antiangiogenic, and antitumor activates. It exerts therapeutic effects via activation/inhibition cellular and molecular targets involved in various diseases, such as retinal diseases. Increasing evidence revealed that curcumin can be used as a therapeutic option in the treatment of different retinal diseases. Here, we summarized various clinical and preclinical studies that used curcumin as a therapeutic agent in the treatment of retinal disorders.