Upregulation of miR-618 contributes to neonatal acute respiratory distress syndrome through BCL2

Neonatal acute respiratory distress syndrome (NARDS) is a potentially fatal condition. This study investigates the role of miR-618 in NARDS pathogenesis and prognosis to explore a novel biomarker for disease monitoring. 110 NARDS patients and 90 healthy controls were enrolled. Serum miR-618 levels were measured using qRT-PCR. ROC curve, Spearman rank correlation, and Kaplan-Meier curves were used to estimate clinical significance. An LPS-induced A549 cell injury model was established to investigate the biological functions of miR-618. Cell viability, apoptosis, and inflammatory cytokine production were assessed. Target prediction and dual-luciferase reporter assay were employed. Serum miR-618 was elevated in NARDS patients and demonstrated good diagnostic performance. miR-618 positively correlated with disease severity indicators including SNAPPE-II score, oxygenation index, and NICU stay duration. High miR-618 expression was associated with lower 30-day survival. In vitro, miR-618 inhibition restored LPS-induced loss of cell viability, reduced apoptosis, ROS and MDA levels, and decreased TNF-α, IL-1β, and IL-6 secretion, while miR-618 upregulation exacerbated these effects. BCL2 overexpression reversed the detrimental effects induced by miR-618 overexpression. BCL2 was validated as a direct target of miR-618, and BCL2 silencing reversed the protective effects of miR-618 inhibition. miR-618 was enhanced in NARDS. miR-618 was related to disease severity and unfavorable prognosis. In vitro, miR-618 promoted inflammatory injury and apoptosis in LPS-induced A549 cells, at least partly through suppression of BCL2. These findings identify the miR-618/BCL2 axis as a candidate molecular pathway for further investigation in NARDS. Not applicable.