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已发表论文
铁死亡在阻塞性睡眠呼吸暂停综合征患儿腺样体肥大中的作用
Authors Shen Z, Huang J , Chu Y , Zhang X, Xu H, Xu H, Guan J, Gu M
Received 10 September 2025
Accepted for publication 5 December 2025
Published 18 December 2025 Volume 2025:17 Pages 3167—3180
DOI https://doi.org/10.2147/NSS.S566579
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Sarah L Appleton
Zilu Shen,1,* Jingning Huang,2,* Yunqiu Chu,2 Xiaoman Zhang,2 Huajun Xu,2 Hongming Xu,1 Jian Guan,2 Meizhen Gu1
1Department of Otorhinolaryngology Head and Neck Surgery, Shanghai Children’s Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200062, People’s Republic of China; 2Department of Otolaryngology Head and Neck Surgery, Shanghai Sixth People’s Hospital, Shanghai Jiao Tong University, Shanghai, 200233, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Hongming Xu, Department of Otorhinolaryngology Head and Neck Surgery, Shanghai Children’s Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200062, People’s Republic of China, Email xuhongming@188.com Meizhen Gu, Department of Otorhinolaryngology Head and Neck Surgery, Shanghai Children’s Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200062, People’s Republic of China, Email gumz@shchildren.com.cn
Purpose: Obstructive sleep apnea (OSA) is a common sleep disorder in children, with adenoid hypertrophy was recognized as the main cause. While ferroptosis has been linked to adult OSA, its role in children with adenoid hypertrophy remains unclear. Here, we aimed to explore the potential role of ferroptosis in pediatric OSA-associated adenoid hypertrophy.
Methods: We conducted RNA sequencing on adenoid tissues from children with OSA stratified by severity (mild-to-moderate, n=9; severe, n=9). Hub genes were identified by integrating differentially expressed genes (DEGs) with ferroptosis-related genes and constructing a protein–protein interaction (PPI) network. We further validated these findings in an independent cohort and primary cells.
Results: KEGG enrichment analysis revealed significant alterations in ferroptosis-related pathways, including p53 signaling pathway and Glutathione metabolism (p < 0.05). We identified 108 ferroptosis-related DEGs (fold change: 0.45– 6.42, adjusted p < 0.05) and subsequently pinpointed 8 hub genes through PPI network construction and Cytoscape analysis (fold change:0.61– 1.81, adjusted p < 0.05). In clinical sample validation, mild-to-moderate tissues exhibited significant activation of ferroptosis. With the exception of PLA2G7, the expression trends of the other 7 hub DEGs were consistent with the findings from bioinformatics analysis. Moreover, ferroptosis inducers significantly suppressed the proliferation of adenoid primary cells in vitro (inhibition rate ≈70%, p < 0.0001).
Conclusion: This study helps us better understand how ferroptosis contributes to adenoid hypertrophy in children with OSA and also suggests that ferroptosis activation may attenuate disease advancement. Furthermore, the 7 hub genes are proposed as potential biomarkers and drug-binding targets.
Keywords: ferroptosis, adenoid hypertrophy, bioinformatic analysis, obstructive sleep apnea
1Department of Otorhinolaryngology Head and Neck Surgery, Shanghai Children’s Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200062, People’s Republic of China; 2Department of Otolaryngology Head and Neck Surgery, Shanghai Sixth People’s Hospital, Shanghai Jiao Tong University, Shanghai, 200233, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Hongming Xu, Department of Otorhinolaryngology Head and Neck Surgery, Shanghai Children’s Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200062, People’s Republic of China, Email xuhongming@188.com Meizhen Gu, Department of Otorhinolaryngology Head and Neck Surgery, Shanghai Children’s Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200062, People’s Republic of China, Email gumz@shchildren.com.cn
Purpose: Obstructive sleep apnea (OSA) is a common sleep disorder in children, with adenoid hypertrophy was recognized as the main cause. While ferroptosis has been linked to adult OSA, its role in children with adenoid hypertrophy remains unclear. Here, we aimed to explore the potential role of ferroptosis in pediatric OSA-associated adenoid hypertrophy.
Methods: We conducted RNA sequencing on adenoid tissues from children with OSA stratified by severity (mild-to-moderate, n=9; severe, n=9). Hub genes were identified by integrating differentially expressed genes (DEGs) with ferroptosis-related genes and constructing a protein–protein interaction (PPI) network. We further validated these findings in an independent cohort and primary cells.
Results: KEGG enrichment analysis revealed significant alterations in ferroptosis-related pathways, including p53 signaling pathway and Glutathione metabolism (p < 0.05). We identified 108 ferroptosis-related DEGs (fold change: 0.45– 6.42, adjusted p < 0.05) and subsequently pinpointed 8 hub genes through PPI network construction and Cytoscape analysis (fold change:0.61– 1.81, adjusted p < 0.05). In clinical sample validation, mild-to-moderate tissues exhibited significant activation of ferroptosis. With the exception of PLA2G7, the expression trends of the other 7 hub DEGs were consistent with the findings from bioinformatics analysis. Moreover, ferroptosis inducers significantly suppressed the proliferation of adenoid primary cells in vitro (inhibition rate ≈70%, p < 0.0001).
Conclusion: This study helps us better understand how ferroptosis contributes to adenoid hypertrophy in children with OSA and also suggests that ferroptosis activation may attenuate disease advancement. Furthermore, the 7 hub genes are proposed as potential biomarkers and drug-binding targets.
Keywords: ferroptosis, adenoid hypertrophy, bioinformatic analysis, obstructive sleep apnea