Scleral Remodeling in Myopia

项目总结/摘要 近视在美国人口中的流行率不断增长，增加了相关疾病的风险。 致盲性疾病，如青光眼和视网膜脱落。近视的眼睛太长了， 目前还没有可接受的方法来预防、减缓或控制近视发展。越来越多的证据 表明眼轴长度受巩膜中未知的生长和重塑机制调节。 我们的目标是阐明这些机制，并制定一个治疗策略的基础上巩膜交联 (SXL)使用低细胞毒性胶原交联剂的结膜下注射。我们的核心假设 巩膜胶原重塑是近视进展的基础，SXL可用于控制巩膜胶原重塑， 重塑和抑制近视进展。本项目的长期目标是阐明关键增长点， 近视的重塑机制，并提供一种安全有效的治疗方式来控制近视 进展 我们将使用已建立的近视实验模型、创新的成像技术和多尺度 计算模拟工具，以深入了解近视眼巩膜重塑的机制。 我们检验了SXL抑制近视进展同时允许生理性眼睛发育的假设 维持视网膜的结构和功能。我们将利用工程和材料科学的原理， 量化巩膜中的巩膜重塑，并测试巩膜变形增加的假设， 近视发展过程中的不同长度尺度和SXL后的减少。 SXL对巩膜重塑控制的支持可以直接转化为一种新的临床治疗方法 近视的策略即使我们的研究结果不支持安全使用SXL控制近视， 我们获得了关于巩膜生长和重塑的信息，其量化将导致一个全新的 了解近视发展的多尺度机制，并将提供一个强大的 该平台旨在开发替代性近视临床控制模式。

Project Summary/Abstract The prevalence of myopia in the U.S. population is constantly growing, increasing the risk for associated blinding diseases such as glaucoma and retinal detachment. A myopic eye is too long for its own optics and there is currently no accepted method to prevent, slow or control myopia progression. Increasing evidence suggest that the eye's axial length is modulated by unknown growth and remodeling mechanisms in the sclera. Our goal is to elucidate these mechanisms and to develop a treatment strategy based on scleral crosslinking (SXL) using subconjunctival injections of a low cytotoxicity collagen crosslink agent. Our central hypotheses are that scleral collagen remodeling underlies myopia progression, and that SXL can be used to control scleral remodeling and inhibit myopia progression. The long-term goal of this project is to elucidate the key growth and remodeling mechanisms in myopia, and to provide a safe and effective treatment modality to control myopia progression. We will use an established experimental model of myopia, innovative imaging techniques, and multi-scale computational simulation tools to gain insight into the mechanisms that underlies scleral remodeling in myopia. We test the hypothesis that SXL inhibits myopia progression while permitting physiological eye development and maintaining retinal structure and function. We will use principals of engineering and material science to quantify scleral remodeling in the sclera and to test the hypotheses that scleral deformations increase at different length-scales during myopia development and decrease after SXL. Support for scleral remodeling control by SXL could be directly translated to a new clinical treatment strategy for myopia. Even if our results do not support the safe usage of SXL for myopia control, the knowledge we gain about scleral growth and remodeling and its quantification would lead to a completely new understanding of the multi-scale mechanisms underlying myopia development, and would provide a powerful platform to develop alternative clinical control modalities of myopia.