Secondary intraocular lens (IOL) implantation is a common treatment for pediatric aphakia. The accurate prediction of IOL power calculation plays a pivotal role in the postoperative development and improvement of visual function for pediatric secondary IOL implantation. Current IOL power calculation formulas were developed based on data from adult phakic eyes and displayed good performance in adult population. However, the formulas showed poor performance in pediatric aphakic population due to the following reasons: 1) In these pediatric aphakic patients, the unavailability of phakic anterior chamber depth (the distance from corneal epithelium to the anterior surface of the lens) and lens thickness (LT) greatly limits the application of some IOL power calculation formulas. 2) IOL power calculation formulas predict the effective lens position on the basis of in-the-bag IOL implantation, whereas sulcus implantation is more widely used in pediatric secondary implantation. Effective lens position in capsular placement is more posterior to ciliary sulcus IOL placement. When applying the initial IOL power calculated for capsular implantation to sulcus implantation, it can lead to refractive errors. 3) Adult eyes have completed their development, with target refractions often being emmetropic or myopic (-3.00 ~ +1.00 D), while pediatric eyes are still developing, necessitating the calculation of an appropriate hyperopic (+0.50 ~ +12.00 D) target refraction to accommodate refractive changes due to ocular growth.To achieve the predetermined target refractive outcomes, the selection and optimization of IOL power calculation formulas is critically important for pediatric secondary IOL implantation.

Despite advancements in allogeneic hematopoietic stem cell transplantation techniques leading to improved overall survival rates, long-term complications have emerged as the primary contributors to poor prognosis and diminished quality of life. Ocular graft-versus-host disease (oGVHD), a prevalent complication affecting over 50% of patients post-transplantation, frequently manifests as refractory dry eye, often accompanied by keratoconjunctivitis. Patients with oGVHD routinely suffer from visual impairment and a decline in their quality of life.Currently, research into the mechanisms, clinical features, diagnosis, and treatment of oGVHD has progressively deepened. This article reviews the latest advancements in the clinical diagnosis and management of oGVHD. Notably, there is a pressing need for strategies focused on early diagnosis and treatment, as early recognition of oGVHD remains challenging. Existing treatments for oGVHD either exhibit limited efficacy or lack robust clinical evidence to support their use as the best available options.Further research is imperative to develop tiered diagnostic and treatment approaches, including the exploration of novel therapeutic targets and biomarkers for disease detection. Such endeavors hold the promise of enhancing patients' long-term prognosis and quality of life.

SGlutamate is the primary excitatory neurotransmitter in the mammalian central nervous system. Persistent activation of the glutamatergic system can lead to excitotoxicity, resulting in neuronal damage and cell death. Members of the excitatory amino acid transporter (EAAT) family are multi-transmembrane proteins located on the presynaptic membrane, synaptic vesicles, and glial cell membranes. They function as high-affinity, sodium-potassium-dependent transporters, continuously clearing extracellular residual glutamate to maintain normal intra- and extracellular glutamate levels and intracellular redox homeostasis. This process is crucial for protecting cells from excitotoxicity and oxidative stress-induced damage. Dysregulation of EAATs is closely associated with the onset and progression of neurodegenerative diseases in the central nervous system. EAAT family members are widely expressed in retina. Numerous studies have demonstrated that these transporters are extensively involved in the pathogenesis of ocular diseases, including glaucoma, retinal ischemia-reperfusion injury, and age-related macular degeneration, although the specific mechanisms remain to be elucidated. Therefore, this article reviews the physiological functions of EAAT family members and their role in the development and progression of related ophthalmic diseases, providing new perspectives for further understanding the molecular mechanisms underlying these conditions and identifying novel therapeutic targets.

Glaucoma is characterized by the progressive degeneration and loss of retinal ganglion cells (RGC) and their axons,making it one of the most common causes of vision loss. Although the exact underlying mechanisms remain unclear, it is well known that elevated intraocular pressure (IOP) is a major risk factor for the progression of glaucoma. Currently, the primary means of controlling glaucoma involves reducing IOP through medication and surgery. Tafluprost, due to its effective and long-term ability to lower IOP, minimal side effects, high patient compliance, and absence of significant systemic side effects, has become the first-line treatment for primary open-angle glaucoma and ocular hypertension. Recent studies suggest that tafluprost may also have neuroprotective effects beyond its IOP-lowering effects. This article aims to review the pharmacological and potential neuroprotective effects of tafluprost, providing a theoretical basis and research foundation for developing more effective drugs for glaucoma treatment. However, there is still a lack of sufficient clinical evidence to support the neuroprotective effects of tafluprost, and further investigations are required to explore in this field to furnish critical theoretical backing for the development of drugs that target optic nerve protection and facilitate vision restoration through optic nerve regeneration.

Glucocorticoid (GC) is widely used in the treatment of ocular inflammation for its anti-inflammatory propery. However, glucocorticoid-induced glaucoma (GIG) is a common complication, and its pathogenesis has been extensively studied. This review summarizes the crucial role of zinc in GIG and its regulatory mechanisms, highlighting zinc's significant involvement in the pathogenesis of glaucoma. Zinc, the second most abundant transition metal in the human body, is essential for protein structure, enzyme catalysis, and cell signaling regulation. The effects of GC on zinc distribution vary across different tissues and cell types, affecting zinc uptake and release, which may contribute to the pathological processes of glaucoma. Zinc influences the degradation and remodeling of the trabecular meshwork extracellular matrix and the survival and axonal regeneration of retinal ganglion cells, playing complex roles in the pathogenesis of GIG. We discuss available strategies for regulating zinc in vivo, including zinc supplementation and reduction strategies, providing potential therapeutic approaches. Future research should explore the mechanisms of zinc's role in glaucoma and its interaction with glucocorticoids, evaluate the safety and efficacy of zinc supplementation or chelation in glaucoma treatment, and develop novel zinc delivery and chelation systems. These efforts will help fully elucidate the role of zinc in glaucoma and its therapeutic potential, enabling more precise prevention and treatment strategies to improve patient outcomes.

Aims: To explore the point-wise correlations between 10-2 visual field (VF) metrics and macular vessel density, as measured by optical coherence tomography angiography (OCTA), in patients with primary open-angle glaucoma (POAG) and healthy controls. Methods: This retrospective study included 54 participants (18 POAG patients and 36 healthy controls) from the Zhongshan Ophthalmic Center. All participants underwent comprehensive ophthalmic examinations, 10-2 VF, and macular OCTA imaging. The correlation between capillary density (CD) in macular subregions and light sensitivity (LS) at corresponding VF test points was analyzed using Pearson's correlation coefficients. Results: The analysis revealed a significant reduction in CD within the inferior macular regions of glaucomatous eyes. Notably, there were strong point-wise correlations between CD and 10-2 VF, particularly in the inferior region of outer ring (peak r = 0.534, P < 0.001). Conclusion: Point-wise correlations between 10-2 VF and macular CD suggest potential for using CD to predict VF metrics in glaucoma, highlighting the importance of macular microcirculation in disease assessment.

Autoimmune uveitis is one of the most common inflammatory eye diseases leading to blindness globally. Its etiology is primarily associated with autoimmune responses. Patients with this condition often exhibit complex and chronic disease courses, with a high propensity for recurrence. Current treatments mainly involve corticosteroids and immunosuppressive agents, which, despite their effectiveness, entail significant side effects that severely impact patients' vision and quality of life. There are still unresolved questions regarding the etiology and immunopathogenesis of autoimmune uveitis, and traditional high-throughput sequencing techniques fall short of adequately elucidatingits pathogenic mechanisms at the cellular level. With the continuous advancement of single-cell sequencing technology, an increasing number of studies are leveraging this approach to deeply investigate the pathogenesis of autoimmune uveitis, thereby offering new insights for identifying novel diagnostic and therapeutic targets. This paper reviews the latest applications of single-cell sequencing technology in exploring the pathogenesis of autoimmune uveitis. Through the utilization of this technology, researchers can gain a more comprehensive understanding of cellular-level changes in patients, providing robust support for the search for new therapeutic avenues. These studies offer new directions for the diagnosis and treatment of autoimmune uveitis and provide valuable information for the development of future therapeutic strategies and approaches.

Retinal vein occlusion (RVO) is one of the major fundus disorders leading to visual impairment, often triggering retinal ischemia, hemorrhage, fluid leakage, and macular edema, which can lead to vision loss or permanent loss. Currently, the main treatment for RVO secondary to macular edema is intravitreal injection of anti-vascular endothelial growth factor (VEGF) drugs. However, the pathological mechanism of RVO is not limited to VEGF but also involves the action of angiopoietin 2 (Ang-2). In pathological states, Ang-2 further promotes the disease progression of RVO by destabilizing blood vessels, inducing neovascularization, and exacerbating the inflammatory response. Faricimab, as a bispecific antibody drug, can inhibit two key pathological pathways, vascular endothelial growth factor A (VEGF-A) and Ang-2, at the same time, showing potential advantages in improving patients' vision.

Objective: To analyze the clinical manifestations, imaging characteristics, and treatment methods of secondary glaucoma associated with congenital ectropion uveae (CEU). Methods: Observational case series and literature review. A retrospective analysis was conducted on the electronic medical records of patients diagnosed with secondary glaucoma due to CEU at the Zhongshan Ophthalmic Center, Sun Yat-sen University, China. Data collected included demographics, visual acuity, intraocular pressure (IOP), slit-lamp examination, gonioscopy, ultrasound biomicroscopy (UBM), and surgical treatment methods. Postoperative IOP were also collected. A literature review was conducted to summarize the clinical characteristics and treatment outcomes of secondary glaucoma due to CEU. Results: Two male patients with secondary glaucoma due to CEU were included, aged 24 and 11 years, respectively. Both patients had a chronic course of disease affecting the right eye, with no systemic abnormalities. The best-corrected visual acuity was hand motion/40 cm to 0.16, and the average IOP at presentation was 37 mmHg, with an average central anterior chamber depth of 3.45 mm. Clinical examination revealed clear corneas, pupils measuring approximately 5-5.5 mm with brisk light reflexes, and nearly 360° of brownish ectropion of the uveae. The lenses were clear, and fundus examination showed glaucomatous optic disc cupping with a normal retina. In the 24-year-old patient, gonioscopy revealed a wide-open angle with trabecular meshwork pigmentation, while UBM indicated slight posterior bowing of the iris and angle closure at the 7 o'clock position. In the 11-year-old patient, both gonioscopy and UBM showed complete angle closure. Corneal endothelial microscopy was normal in both patients. Both were diagnosed with secondary glaucoma due to CEU in the right eye, with elevated IOP that was uncontrolled by maximal medications. The 24-year-old underwent trabeculectomy with intraoperative use of antimetabolites, while the 11-year-old received a drainage valve implantation with antimetabolites. No significant intraoperative or postoperative complications were observed, and IOP was well controlled over a six-month follow-up period. Conclusions: CEU is characterized by ectropion of the uveae and is frequently associated with secondary glaucoma, which may present as open-angle or angle-closure glaucoma. The effectiveness of IOP-lowering medications is limited, often necessitating surgical intervention. Given that secondary glaucoma due to CEU predominantly affects children and young adults, the use of antimetabolites during glaucoma surgery can yield favorable treatment outcomes.

Objective: with the intention of effective prevention and treatment for retinal vein occlusion (RVO), this meta-analysis was performed systematically, evaluating the risk factors of RVO in East Asia. Methods: PubMed, Web of Science, Cochrane Library, CNKI, Wanfang and VIP databases were searched for studies that reported risk factors of RVO in East Asia, published from the establishment of the database to May 2024. To further filter the articles, NOS evaluation method was utilized to assess the quality of selected articles. After valid data were extracted, Meta-analysis was performed by Review Manager software. Results: a total of 21 literatures were included, including 27561 cases in the RVO group (Case group) and 514578 cases in the NRVO group (Control group). Results of meta-analysis showed that chronic kidney disease [odds ratio (OR)=4.14, 95% confidence interval (CI): (1.86%, 9.24%)], hypertension [OR=4.11, 95% CI: (3.09%, 5.48%)], hyperlipidemia [OR=3.45, 95%CI: (2.32%, 5.12%)], diabetes mellitus [OR=3.00, 95%CI: (1.88%, 4.80%)], homocysteine [OR=0.87, 95%CI: (0.59%, 1.15%)], have statistically significant differences between the RVO group and the NRVO group(P<0.05). Conclusion: the occurrence of RVO is closely related to its risk factors, such as chronic kidney disease, hypertension, hyperlipidemia, diabetes mellitus and high homocysteine. In the process of diagnosis and treatment of RVO, doctors should focus on the above risk factors to prevent the occurrence of the disease.