Introduction: The keloids are fibroproliferative disorder and characterized by abnormal proliferation of fibroblasts. In addition, it had been demonstrated that oxidative stress played an important role in autophagy in human fibrotic disorders. However, few researches about oxidative stress had been performed in keloids. Therefore, we performed this study to identify the oxidative stress related signatures and explore their potential mechanisms in keloids. The differential expression genes (DEGs) are obtained from GEO database, and the oxidative stress related genes (OS-genes) were obtained from GeneCards database. The crossed genes, between DEGs and OS-genes, were named as oxidative stress related differential expression genes (OS-DEGs). Then we selected the key OS-DEG and performed the enrichment analysis, interactive network analysis, immune cell infiltration, and correlation between key OS-DEG and Keloids. Results: A total of 105 DEGs were obtained by crossing the DEGs between GSE7890 and GSE145725. And, CDK1, which was downregulated in keloids, was identified as the key OS-DEG. The functional enrichment showed that CDK1 was mainly associated with lysosome, DNA replication, and cell cycle et al. The Human Protein Atlas database delivered that CDK1 was mainly expressed in normal skin and highly expressed in fibroblasts. In addition, many immune cells, including memory resting CD4+ T cells, memory B cells, and CD8+ T cells, were obtained by immune infiltration analysis. Finally, CDK1 showed a strong association with keloids. Conclusion: CDK1 was first stablished to play vital roles in the pathogenesis and treatment of keloids. However, the specific mechanisms of this gene in keloids have not been researched. Therefore, CDK1 provided novel research targets for further analyses in keloids.