Rising miR-618 Levels Linked to Severity in Neonatal Respiratory Distress Syndrome

Serum levels of the microRNA miR-618 are elevated in newborns with neonatal acute respiratory distress syndrome (NARDS), and higher levels track with more severe disease and poorer short-term survival, according to a study published in BMC Immunology on 22 October 2026. The work, led by Jia Zuo, Juan Ouyang and Wenqing Li, positions the miR-618/BCL2 axis as a candidate molecular pathway for further investigation rather than an established clinical tool.

NARDS is a potentially fatal condition affecting newborns, and the authors set out to explore whether miR-618 could serve as a novel biomarker for disease monitoring. The study enrolled 110 NARDS patients and 90 healthy controls. Serum miR-618 was measured using quantitative reverse-transcription PCR, and the researchers assessed its diagnostic performance with ROC curve analysis.

According to the results, serum miR-618 was elevated in NARDS patients and demonstrated good diagnostic performance. The microRNA also showed positive correlations with several disease severity indicators, including the SNAPPE-II score, the oxygenation index, and the duration of the NICU stay. These are associations measured in a single patient cohort, so they do not by themselves establish miR-618 as a cause of disease severity or as a validated diagnostic standard.

Prognostic data pointed in the same direction. High miR-618 expression was associated with lower 30-day survival, as estimated using Kaplan-Meier curves, and Spearman rank correlation was used to examine relationships with severity measures. The authors conclude that miR-618 was related to disease severity and unfavorable prognosis in this cohort.

To probe biological function, the team turned to laboratory experiments rather than patient tissue. They established an LPS-induced injury model in A549 cells, a human lung-derived cell line, and assessed cell viability, apoptosis, and inflammatory cytokine production. Findings from this cell model should not be read as demonstrated clinical benefits in newborns; they describe mechanisms in a controlled in vitro system.

In those experiments, inhibiting miR-618 restored the LPS-induced loss of cell viability, reduced apoptosis, and lowered levels of ROS and MDA, markers of oxidative stress. Inhibition also decreased secretion of the inflammatory cytokines TNF-α, IL-1β, and IL-6. Conversely, upregulating miR-618 exacerbated these effects, suggesting the microRNA promotes inflammatory injury and apoptosis in this model.

The study also examined BCL2, a gene with a known role in regulating cell survival. Target prediction followed by a dual-luciferase reporter assay validated BCL2 as a direct target of miR-618, meaning the microRNA can act on it directly. In functional terms, BCL2 overexpression reversed the detrimental effects induced by miR-618 overexpression, while BCL2 silencing reversed the protective effects of miR-618 inhibition.

Together, these experiments support the authors’ conclusion that, in vitro, miR-618 promotes inflammatory injury and apoptosis in LPS-induced A549 cells at least partly through suppression of BCL2. The reciprocal rescue experiments—overexpressing BCL2 to counter miR-618, and silencing BCL2 to undo the benefit of miR-618 inhibition—provide the mechanistic core of the paper.

The authors frame these findings as identifying the miR-618/BCL2 axis as a candidate molecular pathway for further investigation in NARDS. Because the clinical data come from a single study population and the mechanistic data come from a cell line model, translating these results into bedside biomarkers or therapies would require additional validation. The article was published as open access, and the version shared carries a note that it is subject to further edits before the final Version of Record.

For now, the study adds miR-618 to a growing list of microRNAs being examined in neonatal respiratory distress research, linking a measurable serum signal to severity scores, survival outcomes, and a defined cell-level mechanism through BCL2.

Subject of Research: The role of miR-618 and its target BCL2 in neonatal acute respiratory distress syndrome

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

Article References: Zuo, J., Ouyang, J., & Li, W. (2026). Upregulation of miR-618 contributes to neonatal acute respiratory distress syndrome through BCL2. BMC Immunology. https://doi.org/10.1186/s12865-026-00922-9

Image Credits: AI Generated

DOI: 10.1186/s12865-026-00922-9

Keywords: miR-618, neonatal acute respiratory distress syndrome, NARDS, BCL2, biomarker, microRNA, apoptosis, inflammation, A549 cells, qRT-PCR, prognosis, BMC Immunology