With the emergence of unmanned plane, autonomous vehicles, face recognition, and language processing, the artificial intelligence (AI) has remarkably revolutionized our lifestyle. Recent studies indicate that AI has astounding potential to perform much better than human beings in some tasks, especially in the image recognition field. As the amount of image data in imaging center of ophthalmology is increasing dramatically, analyzing and processing these data is in urgent need. AI has been tried to apply to decipher medical data and has made extraordinary progress in intelligent diagnosis. In this paper, we presented the basic workflow for building an AI model and systematically reviewed applications of AI in the diagnosis of eye diseases. Future work should focus on setting up systematic AI platforms to diagnose general eye diseases based on multimodal data in the real world.

To compare optical coherence tomography angiography (OCTA) screening parameters of the macula and optic nerve head (ONH) between healthy volunteers and chronic hypertensive patients without hypertensive retinopathy. This was an observational, cross-sectional study. Fifty-seven chronic hypertensive patients without hypertensive retinopathy (22 men and 35 women) and 40 healthy volunteers (17 men and 23 women), ranging in age from 60 to 70 years, were included in this study. Patients and volunteers were divided into three groups and one eye was selected randomly from each participant. Group A comprised patients who had a history of hypertension for >10 years (n = 35); Group B comprised patients who had a history of hypertension for 5-10 years (n = 22); and Group C comprised 40 healthy volunteers who had no history of hypertension. A 3 × 3-mm macula scan and a 4.5 × 4.5-mm ONH scan were performed in each group by OCTA using prototype AngioVue software within the AngioVue device. Vessel density (VD), foveal avascular zone (FAZ) area, choriocapillaris flow area, ONH capillary density, retinal nerve fiber layer (RNFL) thickness, and demographic information were compared among the groups. Macula scans showed that superficial plexus VD was significantly lower in groups A and B than in group C (P < 0.05). In addition, FAZ area was significantly larger in group A than in group C (P < 0.05). Inner retinal layer thickness was significantly thinner in groups A and B than in group C (P < 0.05). In ONH scans, RNFL thickness was significantly thinner in group A than in groups B and C (P < 0.05); it was significantly thinner in group B than in group C (P < 0.05). Inside disc capillary density and peripapillary capillary density were significantly lower (P < 0.05) and greater (P < 0.05), respectively, in groups A and B than in group C. Superficial plexus VD, FAZ area, capillary density, and inner retinal thickness changed significantly in hypertensive patients without hypertensive retinopathy. However, only RNFL thickness was significantly thinner in patients who had >10 years of hypertension, compared to patients who had 5-10 years of hypertension. In addition, OCTA provided a method to prospectively assess changes in retinal microvasculature and thickness, thereby avoiding further long-term retinal damage in hypertensive patients.

Diabetic retinopathy (DR) is a highly tissue-specific neurovascular complication of type 1 and type 2 diabetes mellitus and is among the leading causes of blindness worldwide. Pathophysiological changes in DR encompass neurodegeneration, inflammation, and oxidative stress. Current treatments for DR, including anti-vascular endothelial growth factor, steroids, laser photocoagulation, and vitrectomy have limitations and adverse reactions, necessitating the exploration of novel treatment strategies. This review aims to summarize the current pathophysiology, therapeutic approaches, and available drug-delivery methods for treating DR, and discuss their respective development potentials. Recent research indicates the efficacy of novel receptor inhibitors and agonists, such as aldose reductase inhibitors, angiotensin-converting enzyme inhibitors, peroxisome proliferator-activated receptor alpha agonists, and novel drugs in delaying DR. Furthermore, with continuous advancements in nanotechnology, a new form of drug delivery has been developed that can address certain limitations of clinical drug therapy, such as low solubility and poor penetration. This review serves as a theoretical foundation for future research on DR treatment. While highlighting promising therapeutic targets, it underscores the need for continuous exploration to enhance our understanding of DR pathogenesis. The limitations of current treatments and the potential for future advancements emphasize the importance of ongoing research in this field.

Diabetic microangiopathy is a typical and severe problem in diabetics, including diabetic retinopathy, diabetic nephropathy, diabetic neuropathy, and diabetic cardiomyopathy. Patients with type 2 diabetes and diabetic microvascular complications have significantly elevated levels of Asymmetric dimethylarginine (ADMA), which is an endogenous inhibitor of nitric oxide synthase (NOS). ADMA facilitates the occurrence and progression of microvascular complications in type 2 diabetes through its effects on endothelial cell function, oxidative stress damage, inflammation, and fibrosis. This paper reviews the association between ADMA and microvascular complications of diabetes and elucidates the underlying mechanisms by which ADMA contributes to these complications. It provides a new idea and method for the prevention and treatment of microvascular complications in type 2 diabetes.

Background: This study aimed to identify the gene variants and molecular etiologies in 76 unrelated Chinese families with retinitis pigmentosa (RP).Methods: In total, 76 families with syndromic or nonsyndromic RP, diagnosed on the basis of clinical manifestations, were recruited for this study. Genomic DNA samples from probands were analyzed by targeted panels or whole exome sequencing. Bioinformatics analysis, Sanger sequencing, and available family member segregation were used to validate sequencing data and confirm the identities of disease‐causing genes.Results: The participants enrolled in the study included 62 families that exhibited nonsyndromic RP, 13 that exhibited Usher syndrome, and one that exhibited Bardet–Biedl syndrome. We found that 43 families (56.6%) had disease‐causing variants in 15 genes, including RHO, PRPF31, USH2A, CLRN1, BBS2, CYP4V2, EYS, RPE65, CNGA1, CNGB1, PDE6B, MERTK, RP1, RP2, and RPGR; moreover, 12 families (15.8%) had only one heterozygous variant in seven autosomal recessive RP genes, including USH2A, EYS, CLRN1, CERKL, RP1, CRB1, and SLC7A14. We did not detect any variants in the remaining 21 families (27.6%). We also identified 67 potential pathogenic gene variants, of which 24 were novel.Conclusion: The gene variants identified in this study expand the variant frequency and spectrum of RP genes; moreover, the identification of these variants supplies foundational clues for future RP diagnosis and therapy.