EMX2OS serves as a biomarker of neonatal sepsis and participates acute lung injury through enhancing ferroptosis
Year: 2025
Type: article
Abstract: 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.
Source: Frontiers in Pediatrics
Authors: Xuexiang Li, Zhiqiang Liu, Guilian Shan, Lili Shi, Zhihua Liu
Institution: Shengli Oilfield Central Hospital
Language: English
Subfield: Pulmonary and Respiratory Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $3,801
OpenAlex ID: W4414148145