Unveiling the role of EGR1 and hub senescencerelated genes in Type II alveolar epithelial cells senescence for Obstructive sleep Apnea

Backgroud : A frequently encountered breathing condition, obstructive sleep apnea (OSA) primarily manifests while sleeping and is characterized by total or incomplete blockage of the upper respiratory tract. This disorder disrupts normal airflow, often leading to repeated pauses in breathing throughout the night. Aging significantly increases the risk of OSA, yet the underlying biomolecular connections between aging and OSA remain incompletely understood. Methods : This research integrates bioinformatics and machine learning methods. To discover and confirm possible biomarkers, a combination of WGCNA and machine learning techniques was utilized. Functional characterization of genes was achieved through GO and KEGG enrichment studies, which provided insights into biological pathways and molecular roles. A predictive nomogram was developed based on hub hub OSA-ARDEGs.Comprehensive immune infiltration analysis was conducted to elucidate the immunological microenvironment associated with key biomarkers.To experimentally validate computational predictions, RNA-seq and Western blotting analyses were performed to confirm EGR1 expression patterns in human type II alveolar epithelial cells. Results : Investigative studies revealed genes exhibiting differential expression patterns, along with interconnected gene networks that showed notable associations with OSA. The analysis further demonstrated that these molecular networks are intricately tied to mechanisms of biological aging and immune system activity. Enrichment studies revealed that these genes are involved in multiple biological mechanisms, including processes related to inflammation and signaling cascades mediated by immune cells. Furthermore, EGR1 was validated experimentally as a critical gene involved in cellular senescence, immune regulation, and DNA damage response. Conclusion : Our findings establish EGR1 as a crucial mediator in OSA pathogenesis, potentially driving disease progression through cellular senescence mechanisms. These results position EGR1 as a promising molecular target for developing therapeutic interventions against OSA-associated respiratory dysfunction.