Xuexiang Li, Zhiqiang Liu, Guilian Shan, Lili Shi, Zhihua Liu
{"title":"EMX2OS作为新生儿脓毒症的生物标志物，通过增强铁下沉参与急性肺损伤。","authors":"Xuexiang Li, Zhiqiang Liu, Guilian Shan, Lili Shi, Zhihua Liu","doi":"10.3389/fped.2025.1654832","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Neonatal Sepsis (NS) is an important cause of neonatal death, often accompanied by acute lung injury (ALI). Ferroptosis plays a role in infectious diseases, but its regulatory mechanism in NS-related ALI remains unclear. The aim of this study is to investigate the mechanism of EMX2OS in promoting ferroptosis in ALI.</p><p><strong>Methods: </strong>The expression level of EMX2OS in peripheral blood of patients with NS and its diagnostic value were detected by clinical samples. LPS-induced A549 cells were used to establish an ALI model. The targeting relationship between EMX2OS, miR-654-3p and AKT3 was verified by qRT-PCR, CCK-8, detection kit and dual-luciferase assays, and the cell viability and ferroptosis level were evaluated.</p><p><strong>Results: </strong>EMX2OS was highly expressed in NS and served as a potential diagnostic marker. In LPS-induced lung injury model, high expression of EMX2OS decreased cell viability and enhanced ferroptosis. Silencing EMX2OS had the opposite effects. EMX2OS regulated cell viability and ferroptosis through miR-654-3p/AKT3 axis.</p><p><strong>Conclusions: </strong>This study reveals for the first time that EMX2OS serves as a diagnostic marker for NS and promotes ferroptosis through miR-654-3p/AKT3 axis, thereby exacerbating lung injury. EMX2OS to regulate ferroptosis may become potential therapeutic strategies for lung injury.</p>","PeriodicalId":12637,"journal":{"name":"Frontiers in Pediatrics","volume":"13 ","pages":"1654832"},"PeriodicalIF":2.0000,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12454030/pdf/","citationCount":"0","resultStr":"{\"title\":\"EMX2OS serves as a biomarker of neonatal sepsis and participates acute lung injury through enhancing ferroptosis.\",\"authors\":\"Xuexiang Li, Zhiqiang Liu, Guilian Shan, Lili Shi, Zhihua Liu\",\"doi\":\"10.3389/fped.2025.1654832\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Neonatal Sepsis (NS) is an important cause of neonatal death, often accompanied by acute lung injury (ALI). Ferroptosis plays a role in infectious diseases, but its regulatory mechanism in NS-related ALI remains unclear. The aim of this study is to investigate the mechanism of EMX2OS in promoting ferroptosis in ALI.</p><p><strong>Methods: </strong>The expression level of EMX2OS in peripheral blood of patients with NS and its diagnostic value were detected by clinical samples. LPS-induced A549 cells were used to establish an ALI model. The targeting relationship between EMX2OS, miR-654-3p and AKT3 was verified by qRT-PCR, CCK-8, detection kit and dual-luciferase assays, and the cell viability and ferroptosis level were evaluated.</p><p><strong>Results: </strong>EMX2OS was highly expressed in NS and served as a potential diagnostic marker. In LPS-induced lung injury model, high expression of EMX2OS decreased cell viability and enhanced ferroptosis. Silencing EMX2OS had the opposite effects. EMX2OS regulated cell viability and ferroptosis through miR-654-3p/AKT3 axis.</p><p><strong>Conclusions: </strong>This study reveals for the first time that EMX2OS serves as a diagnostic marker for NS and promotes ferroptosis through miR-654-3p/AKT3 axis, thereby exacerbating lung injury. EMX2OS to regulate ferroptosis may become potential therapeutic strategies for lung injury.</p>\",\"PeriodicalId\":12637,\"journal\":{\"name\":\"Frontiers in Pediatrics\",\"volume\":\"13 \",\"pages\":\"1654832\"},\"PeriodicalIF\":2.0000,\"publicationDate\":\"2025-09-09\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12454030/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Frontiers in Pediatrics\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.3389/fped.2025.1654832\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q2\",\"JCRName\":\"PEDIATRICS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Frontiers in Pediatrics","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3389/fped.2025.1654832","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"PEDIATRICS","Score":null,"Total":0}
EMX2OS serves as a biomarker of neonatal sepsis and participates acute lung injury through enhancing ferroptosis.
Background: Neonatal Sepsis (NS) is an important cause of neonatal death, often accompanied by acute lung injury (ALI). Ferroptosis plays a role in infectious diseases, but its regulatory mechanism in NS-related ALI remains unclear. The aim of this study is to investigate the mechanism of EMX2OS in promoting ferroptosis in ALI.
Methods: The expression level of EMX2OS in peripheral blood of patients with NS and its diagnostic value were detected by clinical samples. LPS-induced A549 cells were used to establish an ALI model. The targeting relationship between EMX2OS, miR-654-3p and AKT3 was verified by qRT-PCR, CCK-8, detection kit and dual-luciferase assays, and the cell viability and ferroptosis level were evaluated.
Results: EMX2OS was highly expressed in NS and served as a potential diagnostic marker. In LPS-induced lung injury model, high expression of EMX2OS decreased cell viability and enhanced ferroptosis. Silencing EMX2OS had the opposite effects. EMX2OS regulated cell viability and ferroptosis through miR-654-3p/AKT3 axis.
Conclusions: This study reveals for the first time that EMX2OS serves as a diagnostic marker for NS and promotes ferroptosis through miR-654-3p/AKT3 axis, thereby exacerbating lung injury. EMX2OS to regulate ferroptosis may become potential therapeutic strategies for lung injury.
期刊介绍：
Frontiers in Pediatrics (Impact Factor 2.33) publishes rigorously peer-reviewed research broadly across the field, from basic to clinical research that meets ongoing challenges in pediatric patient care and child health. Field Chief Editors Arjan Te Pas at Leiden University and Michael L. Moritz at the Children''s Hospital of Pittsburgh are supported by an outstanding Editorial Board of international experts. This multidisciplinary open-access journal is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics, clinicians and the public worldwide.
Frontiers in Pediatrics also features Research Topics, Frontiers special theme-focused issues managed by Guest Associate Editors, addressing important areas in pediatrics. In this fashion, Frontiers serves as an outlet to publish the broadest aspects of pediatrics in both basic and clinical research, including high-quality reviews, case reports, editorials and commentaries related to all aspects of pediatrics.
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