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已发表论文
ARDS 中铁死亡相关生物标志物和治疗靶点的识别与验证：一项生物信息学和实验研究
Authors Dong B , Zhong B, Zuo J, Liao L , Zeng W, Xiong M, Wei Y, Zhang D, Fan X
Received 24 September 2025
Accepted for publication 24 March 2026
Published 21 April 2026 Volume 2026:19 566825
DOI https://doi.org/10.2147/JIR.S566825
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Cynthia Koziol-White
Biying Dong,1– 4,* Bing Zhong,1,2,* Jing Zuo,5,* Longxiong Liao,1– 4 Weitong Zeng,3,4 Minjun Xiong,3 Yi Wei,3,4 Dongwei Zhang,3,4 Xianming Fan1,2
1Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, People’s Republic of China; 2Inflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, People’s Republic of China; 3Department of Respiratory and Critical Care Medicine, Liuzhou People’s Hospital, Guangxi Medical University, Liuzhou, Guangxi, People’s Republic of China; 4Key Laboratory of Diagnosis, Treatment and Research of Asthma and Chronic Obstructive Pulmonary Disease, Liuzhou, Guangxi, People’s Republic of China; 5Department of Pulmonary Disease, Jiang ‘an County Hospital of Traditional Chinese Medicine, Yibin, Sichuan, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Dongwei Zhang, Department of Respiratory and Critical Care Medicine, Liuzhou People’s Hospital, Guangxi Medical University, No. 8, Wenchang Road, Yufeng District, Liuzhou, Guangxi Province, 545006, People’s Republic of China, Email zhangdongwei2003@126.com Xianming Fan, Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Southwest Medical University, 25 Taiping Street, Jiangyang District, Luzhou, Sichuan Province, 646000, People’s Republic of China, Email fxm129@swmu.edu.cn
Background: Acute respiratory distress syndrome (ARDS) is a severe inflammatory lung disease with high mortality and limited effective therapies. Recent studies link ferroptosis—an iron-dependent regulated cell death—to ARDS pathogenesis. This study aimed to identify/validate ferroptosis-related diagnostic biomarkers, therapeutic targets, and fecal microbiota transplantation (FMT)’s protective role in ARDS.
Methods: Bioinformatic analyses of GEO datasets (GSE76293/GSE151263) included differential expression profiling, WGCNA, PPI network, and machine learning (LASSO/RF) to screen hub genes, with ROC analysis for diagnostic efficacy. An LPS-induced ARDS rat model with FMT intervention was validated via qRT-PCR, IHC, Western blot, and histological staining.
Results: Thirty-seven ferroptosis-linked differentially expressed genes (FDEGs) were identified, enriched in ferroptosis, mitophagy, and immune pathways. Three hub genes (MAPK8, CREB1, GPX4) showed robust diagnostic utility (LASSO AUC=0.931; RF AUC=0.993 in GSE76293) and correlated with monocytes/neutrophils/activated NK cells. LPS suppressed their mRNA/protein levels in rats, reversed by FMT.
Conclusion: MAPK8, CREB1, and GPX4 are potential diagnostic biomarkers and therapeutic targets for ARDS. FMT protects against ARDS by reversing these genes’ downregulation and suppressing ferroptosis, providing new insights into ARDS pathogenesis and ferroptosis-targeted interventions.
Keywords: acute respiratory distress syndrome, ferroptosis, fecal microbiota transplantation, GPX4, MAPK8, CREB1
1Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, People’s Republic of China; 2Inflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, People’s Republic of China; 3Department of Respiratory and Critical Care Medicine, Liuzhou People’s Hospital, Guangxi Medical University, Liuzhou, Guangxi, People’s Republic of China; 4Key Laboratory of Diagnosis, Treatment and Research of Asthma and Chronic Obstructive Pulmonary Disease, Liuzhou, Guangxi, People’s Republic of China; 5Department of Pulmonary Disease, Jiang ‘an County Hospital of Traditional Chinese Medicine, Yibin, Sichuan, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Dongwei Zhang, Department of Respiratory and Critical Care Medicine, Liuzhou People’s Hospital, Guangxi Medical University, No. 8, Wenchang Road, Yufeng District, Liuzhou, Guangxi Province, 545006, People’s Republic of China, Email zhangdongwei2003@126.com Xianming Fan, Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Southwest Medical University, 25 Taiping Street, Jiangyang District, Luzhou, Sichuan Province, 646000, People’s Republic of China, Email fxm129@swmu.edu.cn
Background: Acute respiratory distress syndrome (ARDS) is a severe inflammatory lung disease with high mortality and limited effective therapies. Recent studies link ferroptosis—an iron-dependent regulated cell death—to ARDS pathogenesis. This study aimed to identify/validate ferroptosis-related diagnostic biomarkers, therapeutic targets, and fecal microbiota transplantation (FMT)’s protective role in ARDS.
Methods: Bioinformatic analyses of GEO datasets (GSE76293/GSE151263) included differential expression profiling, WGCNA, PPI network, and machine learning (LASSO/RF) to screen hub genes, with ROC analysis for diagnostic efficacy. An LPS-induced ARDS rat model with FMT intervention was validated via qRT-PCR, IHC, Western blot, and histological staining.
Results: Thirty-seven ferroptosis-linked differentially expressed genes (FDEGs) were identified, enriched in ferroptosis, mitophagy, and immune pathways. Three hub genes (MAPK8, CREB1, GPX4) showed robust diagnostic utility (LASSO AUC=0.931; RF AUC=0.993 in GSE76293) and correlated with monocytes/neutrophils/activated NK cells. LPS suppressed their mRNA/protein levels in rats, reversed by FMT.
Conclusion: MAPK8, CREB1, and GPX4 are potential diagnostic biomarkers and therapeutic targets for ARDS. FMT protects against ARDS by reversing these genes’ downregulation and suppressing ferroptosis, providing new insights into ARDS pathogenesis and ferroptosis-targeted interventions.
Keywords: acute respiratory distress syndrome, ferroptosis, fecal microbiota transplantation, GPX4, MAPK8, CREB1