The prevalence of myopia is rapidly increasing, significantly impacting the quality of life for affected individuals. Prior research in our group observed reactive gliosis in Müller cells within myopia-induced retinas, prompting further investigation into their role in myopia. In this study, we analyzed protein expression changes in CD29+ Müller cells, isolated using magnetic activated cell sorting (MACS), from form deprivation myopia-induced rabbit retina. These cells, the principal glial cells in the retina, showed significant alterations in metabolic pathways, particularly in glycolysis and angiogenesis, including the upregulation of glycolytic enzymes such as lactate dehydrogenase A and pyruvate kinase. These enzymes are implicated in adapting to increased metabolic demands under myopic stress. Additionally, a decrease in proteins associated with oxygen transport suggests an enhanced vulnerability to oxidative stress. Our findings highlight the proactive role of CD29+ Müller cells in modifying the retinal environment in response to myopic stress, suggesting potential therapeutic targets to mitigate myopia’s progression.