The cornea is a vital component of the visual system, and its integrity is crucial for optimal vision. Damage to the cornea resulting from trauma, infection, or disease can lead to blindness. Corneal regeneration using mesenchymal stem cells (MSCs) and MSC-derived extracellular vesicles (MSC-EVs) offers a promising alternative to corneal transplantation. MSCs are multipotent stromal cells that can differentiate into various cell types, including corneal cells. They can also secrete a variety of anti-inflammatory cytokines and several growth factors, promoting wound healing and tissue reconstruction. This review summarizes the current understanding of the molecular and cellular mechanisms by which MSCs and MSC-EVs contribute to corneal regeneration. It discusses the potential of MSCs and MSC-EV for treating various corneal diseases, including corneal epithelial defects, dry eye disease, and keratoconus. The review also highlights finalized human clinical trials investigating the safety and efficacy of MSC-based therapy in corneal regeneration. The therapeutic potential of MSCs and MSC-EVs for corneal regeneration is promising; however, further research is needed to optimize their clinical application.

We reviewed the current state of knowledge regarding visual function and its suitability as part of medical examinations for driving licenses. We focused only on Group 1 drivers. According to previous studies, visual acuity, which is the most common test, is weakly associated with a higher risk of road accidents, with a greater role of visual field. The inclusion of the visual field test in medical examinations is therefore important, but the actual limit value is still unclear and further research in specific situations is needed. Color vision impairment was not found a threat to traffic safety. Contrast sensitivity decreases with age and is affected by abnormal eye conditions. Resulting glare can lead to an increased risk of traffic accidents during night driving in the elderly and others with conditions that impair contrast sensitivity. However, the universal cut-off limits have not been established either. The current European Union (EU) regulations therefore reflect minimum common denominator across the member states which may not entirely translate to optimal driving safety. Due to these open questions, standardized testing in simulators or on polygons that simulate real life conditions would be needed to better determine safe limits of visual function in different conditions. As there is a need to have better standardization across Europe regarding the requirements and rules regarding driving licenses in European countries, we first analyzed existing rules and compared them with each other, also in terms of deviations from the EU directive itself. We reviewed the literature in this field and prepared proposals for a more optimal regulation of the rules in the future. Particular attention is paid to the new method of examining the visual field that was created to respect the European directive. The paper can serve as a basis of information for research teams to design further protocols, as it gathers research findings to date on the importance and impact of various visual functions on driving safety, as well as a starting point for a debate on revising existing rules for obtaining and maintaining licenses, as it compares the current regulations in European countries and differences between them.

Mutations in rhodopsin gene (RHO) are a frequent cause of retinitis pigmentosa (RP) and less often, congenital stationary night blindness (CSNB). Mutation p.G90D has previously been associated with CSNB based on the examination of one family. This study screened 60 patients. Out of these 60 patients, 32 were affected and a full characterization was conducted in 15 patients. We described the clinical characteristics of these 15 patients (12 male, median age 42 years, range 8–71) from three families including visual field (Campus Goldmann), fundus autofluorescence (FAF), optical coherence tomography (OCT) and electrophysiology. Phenotypes were classified into four categories: CSNB (N = 3, 20%) sector RP (N = 3, 20%), pericentral RP (N = 1, 6.7%) and classic RP (N = 8, 53.3% (8/15)). The phenotypes were not associated with family, sex or age (Kruskal–Wallis, p > 0.05), however, cystoid macular edema (CME) was observed only in one family. Among the subjects reporting nyctalopia, 69% (22/32) were male. The clinical characteristics of the largest p.G90D cohort so far showed a large frequency of progressive retinal degeneration with 53.3% developing RP, contrary to the previous report.

The pathogenic variant p.G90D in RHO is believed to be responsible for a spectrum of phenotypes, including congenital stationary blindness (for the purpose of this study termed night blindness without degeneration; NBWD), Sector RP, Pericentral RP, and Classic RP. We present a correlation between the serum concentration of vitamin A and disease severity in patients with this variant. This prospective study involved 30 patients from 7 families (17 male; median age 46 years, range 8–73). Full ophthalmological examination including visual acuity, Goldmann perimetry, slit-lamp exam, optical coherence tomography, fundus autofluorescence, and electrophysiology was performed to determine the presenting phenotype. The serum concentration of vitamin A was determined from a fasting blood sample taken on the day of the exam, where it was found that 23.3% (7/30) of patients had NBWD, 13.3% (4/30) had Sector RP, 3.3% (1/30) had Pericentral RP, and 60% (18/30) had Classic RP. Multiple logistic regression revealed a significantly higher probability of having a milder phenotype (NBWD or Sector RP) in association with younger age (p < 0.05) and a higher concentration of vitamin A (p < 0.05). We hypothesize that vitamin A in its 11-cis-retinal form plays a role in stabilizing the constitutively active p.G90D rhodopsin and its supplementation could be a potential treatment strategy for p.G90D RHO patients.

Objective: Rho-associated protein kinase (ROCK) inhibitors have recently emerged as promising agents for the treatment of corneal endothelial dysfunction. Because corneal transparency critically depends on endothelial cell function, endothelial failure can lead to persistent visual impairment. However, clinical evidence regarding the use of topical ROCK inhibition in various etiologies of endothelial decompensation remains limited. The aim of this study was to evaluate changes in central corneal thickness (CCT), best-corrected visual acuity (BCVA), and treatment-related adverse events in eyes with corneal edema of different etiologies treated with fixed-combination drops of netarsudil 0.02%/latanoprost 0.005%, Roclanda^®. Methods: In this prospective, uncontrolled, exploratory case series, we investigated the effects of topical ROCK inhibition on corneal endothelial cell function in 13 eyes of 11 patients with persistent, nonhealing corneal edema following intraocular procedures. Patients were treated with topical Roclanda^® once daily for three months. Clinical evaluation included BCVA, CCT, and safety assessment. Changes in CCT and BCVA were assessed before therapy, and after 1 and 3 months of treatment. Results: Mean baseline CCT was 782.8 µm and decreased significantly by 71.0 µm at 1 month and by 120.2 µm at 3 months (p = 0.0074 and 0.0012, respectively). Complete resolution of corneal edema was achieved in 38% of eyes. Mean BCVA improved from 0.744 before treatment to 0.518 logMAR at 3 months (p = 0.0026), with 46.2% of eyes gaining two or more Snellen lines. The analysis including only one eye per patient showed similar results, with statistically significant reductions in CCT at both 1 and 3 months and a significant improvement in BCVA at 3 months after the exclusion of the second eye in bilaterally included patients. Treatment was well tolerated; with mild conjunctival hyperemia as the most common adverse effect, while reticular epithelial corneal edema occurred in one eye and resolved after the completion of the treatment. Conclusions: In this prospective, exploratory case series of patients with nonhealing corneal edema, 3 months of a fixed-dose netarsudil 0.02%/latanoprost 0.005% treatment resulted in significant reduction in CCT, as well as clinically important improvement in BCVA. These exploratory findings cannot explain the mechanism of action, but suggest a potential therapeutic role for ROCK inhibitors in eyes with nonhealing corneal edema and possibly residual endothelial reserve. Larger controlled studies are needed to confirm these observations and further define indications for treatment.