ArticleFrontiers in surgery2026
Decoding the cGAS-STING-eosinophils predictive and natural therapeutic molecular signature in burn injury progression and keloid formation: insights from artificial intelligence-driven multiomics.
Article in Frontiers in surgery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Inflammation-related pathway activation contributes to the progression of burn injury and keloid formation. Objective: Our study aimed to investigate the role of the cGAS-STING pathway in regulating eosinophils during the progression of burn injury and keloid formation. Methods: Key cGAS-STING pathway and eosinophils (CE)-related differentially expressed genes (DEGs) were identified in burn injury patient bulk profiles (GSE19743) using Limma, WGCNA, CIBERSORT, and STRING frameworks. Next, a systemic and explainable machine learning model was utilized to identify predictive model hub genes involved in keloid formation of burn injury patients (GSE37069) and burn-injury-associated keloid patient (GSE42270), based on CE-associated DEGs. The pathogenic role of hub genes and eosinophils in keloid formation was further assessed in a keloid patient single-cell profile (GSE243716) using cutting-edge single-cell analytical frameworks, such as AUCELL, sctenifoldknk, and Bayesprism. In addition, a deep learning algorithm (DrugRefLector) and molecular docking were employed to identify natural compounds targeting the hub gene for the treatment of burn-injury-associated keloid (GSE42270). Finally, Results: An integrated CE-associated gene signature can indicate keloid formation in burn injury patients. CCL5 can be considered as an up-regulated pathogenic factor and therapeutic target for Icariin, which is involved in keloid pathogenesis. Conclusion: This is the first study to identify a CA-associated signature in keloid formation among burn injury patients.
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