ArticleBMC immunology2026
Investigating the role of miR-192-5p as a diagnostic biomarker and the anti-inflammatory function in pediatric acute respiratory distress syndrome.
Article in BMC immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundHigh mortality of pediatric acute respiratory distress syndrome (PARDS) demands new biomarkers.
aimThe study aims to clarify the clinical value of miR-192-5p in PARDS and its regulatory role in inflammatory responses.
methodsBaseline data and serum samples were collected from healthy children, sepsis children, and sepsis-induced PARDS subjects. The receiver operating characteristic curve (ROC), Kaplan-Meier curve and multivariate Cox regression were used to assess miR-192-5p’s diagnostic and prognostic value for PARDS. The relationship between miR-192-5p and each index was evaluated by correlation analysis. The expression of miR-192-5p, inflammatory factors and ZEB2 in the subjects’ serum and human pulmonary microvascular endothelial cells (HPMECs) were detected by RT-qPCR. The cell viability and secretion of inflammatory factors were evaluated by CCK-8 and ELISA kit. Bioinformatic prediction combined with dual-luciferase reporter assay was used to verify the target genes.
resultsmiR-192-5p was significantly low-expressed in PARDS patients’ serum. MiR-192-5p was a prognostic protective factor for PARDS, and low miR-192-5p indicated poor prognosis. MiR-192-5p was negatively correlated with TNF-α, IL-6, IL-1β, and APACHE II score. LPS treatment led to reduced HPMECs viability, excessive inflammatory factor production, and down-regulated miR-192-5p expression. Overexpression of miR-192-5p mimic could partially reverse the above phenomena, while knockdown could aggravate the above phenomena. ZEB2 was a downstream target gene of miR-192-5p.
conclusionsmiR-192-5p serves as a diagnostic biomarker for PARDS and links to poor prognosis. Downregulation of miR-192-5p may promote LPS-induced inflammatory response and induce HPMECs cell viability by targeting ZEB2, thereby involving in the progression of PARDS.
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