Refractive errors, particularly myopia, are among the most prevalent visual impairments globally, with rising incidence in children and adolescents. This review explores the epidemiology and risk factors associated with the development of refractive errors, focusing on the environmental and lifestyle factors contributing to the current surge in myopia. We provide an overview of key genetic factors and molecular pathways driving the pathogenesis of myopia and other refractive errors, emphasizing the complex interplay between genetic predisposition and environmental triggers. Understanding the underlying mechanisms is crucial for identifying new strategies for intervention. We discuss current approaches to slow myopia progression in pediatric populations, including pharmacological treatment regimens (low-dose atropine), optical interventions, and lifestyle modifications. In addition to established therapies, we highlight emerging innovations, including new pharmacological agents and advanced optical devices, and insights into potential future treatments. Cutting-edge research into gene therapy, molecular inhibitors, and neuroprotective strategies may yield novel therapeutic targets that address the root causes of refractive errors. This comprehensive review underscores the importance of early intervention and highlights promising avenues for future research, aiming to provide pediatricians with guidance to ultimately improve clinical outcomes in managing and preventing myopia progression in children and young adults.
Purpose: While the first murine endothelial keratoplasty (EK) model established surgical feasibility, manual lamellar dissection and endothelial scraping introduce significant procedural variability. This study aims to develop a standardized murine EK model implementing a controlled stromal peeling technique and quadrant-based host bed preparation to minimize inconsistency. Methods: We introduced 2 critical methodological refinements. First, donor corneas were prepared using a controlled stromal peeling approach to ensure uniform graft thickness. Second, traditional circular scraping of the recipient endothelium was replaced with quadrant-based mechanical removal to standardize the denuded area. Postoperative outcomes were quantified using AS-OCT and a novel time-resolved opacity scoring system designed to distinguish early technical failure from immunologic rejection. Results: Controlled stromal peeling produced posterior lamellar grafts with significantly higher thickness consistency compared with traditional needle dissection. The quadrant-based removal resulted in highly reproducible postoperative corneal edema, reflecting standardized disruption of host endothelial function. Furthermore, the time-resolved grading system allowed more granular, objective differentiation between early graft failure and delayed rejection compared with traditional binary survival assessments. Conclusions: These refinements overcome the inherent variability of the initial murine EK model. By standardizing both the surgical procedure and the interpretive framework, this optimized model provides a robust, reproducible platform for investigating cellular mechanisms of graft outcomes in experimental keratoplasty.