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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.