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Red light therapy has shown promising effects in the treatment of myopia in children. One of the underlying causes of myopia is structural changes in the sclera, which lead to axial elongation of the eye. However, the effects of red light on scleral remodeling in myopic patients remain unclear. In this study, we used a headcap-based form-deprivation myopia (FDM) model in guinea pigs to establish experimental groups for red light treatment and control. Following the transcriptome sequencing of scleral tissue from different groups, differential gene expression and pathway clustering analyses were performed. The result revealed that the expression of the CCDC152 gene were associated with the formation of myopia and the effects of red light treatment. In primary fibroblasts isolated from the sclera, overexpression of CCDC152 confirmed its inhibitory role in red light therapy. Our results suggest that red light exposure can partially restore refractive error and axial length in myopic guinea pigs, and may slow the progression of myopia by delaying scleral remodeling. CCDC152 may act as an "oxidant," potentially disrupting scleral structure through oxidative stress, thereby negatively affecting red light therapy. Red light therapy effectively modulates GPCR pathways in the retina, alleviating stress and influencing the development of myopia.

红光疗法在儿童近视治疗中已展现出良好应用前景。近视的潜在诱因之一为巩膜结构改变，进而引发眼轴延长。但目前红光对近视患者巩膜重塑的具体作用机制仍不明确。本研究采用基于头罩的形觉剥夺性近视（form-deprivation myopia, FDM）豚鼠模型，设立红光治疗组与对照组。对各组巩膜组织进行转录组测序后，开展了差异基因表达分析与通路聚类分析。研究结果显示，CCDC152基因的表达水平与近视形成及红光治疗效果密切相关。在从巩膜分离的原代成纤维细胞中，过表达CCDC152验证了其在红光治疗中的抑制作用。本研究结果表明，红光照射可部分恢复近视豚鼠的屈光不正与眼轴长度，并通过延缓巩膜重塑以减缓近视进展。CCDC152可作为"氧化剂"，通过氧化应激破坏巩膜结构，进而对红光治疗产生负面影响。红光疗法可有效调控视网膜内的G蛋白偶联受体（G protein-coupled receptor, GPCR）通路，缓解应激反应并影响近视发生发展。