Scleral Remodeling in Myopia

项目摘要/摘要 近视在美国人口中的流行率不断增长，增加了与近视相关的风险 青光眼和视网膜脱离等致盲疾病。近视的眼睛对于它自己的光学来说太长了，而且 目前还没有公认的方法来预防、减缓或控制近视进展。越来越多的证据 提示眼轴长度受未知的巩膜生长和重塑机制的调节。 我们的目标是阐明这些机制，并开发一种基于巩膜交联的治疗策略。 (SXL)使用结膜下注射一种低细胞毒性的胶原交联剂。我们的中心假设 巩膜胶原重塑是近视进展的基础，并且SXL可用于控制巩膜吗 重塑和抑制近视进展。该项目的长期目标是阐明关键的增长和 近视的重塑机制，为控制近视提供一种安全有效的治疗方法 进步。 我们将使用已建立的近视实验模型，创新的成像技术，以及多尺度 计算机模拟工具，以深入了解近视巩膜重塑的机制。 我们验证了SXL在抑制近视进展的同时允许生理眼睛发育的假设 并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来 量化巩膜重塑并检验巩膜变形增加的假说 近视发生发展过程中的不同长度尺度，SXL术后近视长度尺度减小。 SXL对巩膜重塑控制的支持可直接转化为一种新的临床治疗方法 近视的策略。即使我们的结果不支持SXL用于近视控制的安全使用，知识 我们得到了关于巩膜生长和重塑的信息，它的量化将导致一个全新的 了解近视发生的多尺度机制，将提供强大的 开发近视替代临床控制模式的平台。

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.