ArticleBMC immunology2026
Upregulation of miR-223 by SIRT1 attenuates the inflammatory response in neonatal sepsis.
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.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe diversity of clinical symptoms of neonatal sepsis leads to difficulties in diagnosis, and the treatment is limited. This study aims to investigate the role of the SIRT1/miR-223 signaling axis in neonatal sepsis.
methods100 neonates with sepsis and 100 healthy infants were included in this study. The RT-qPCR was used to detect RNA and inflammatory factor levels in serum. Peripheral blood neutrophils were isolated by gradient centrifugation. LPS-stimulated neutrophils were detected for MPO activity and inflammatory factor expression. Neutrophils were transfected with miR-223 oligonucleotide and SIRT1-related plasmid to detect changes in neutrophil-related parameters.
resultsNeonates with sepsis had a significantly stronger inflammatory response than healthy infants, and the expression of miR-223 and SIRT1 in the serum was remarkably reduced. ROC curves showed that miR-223 had a diagnostic value for neonatal sepsis. The expression of miR-223 and SIRT1 was notably reduced in the model cells, and overexpression of miR-223 attenuated the inflammatory response in the LPS-induced neutrophil. Overexpression of SIRT1 could alleviate the enhanced inflammatory response due to inhibition of miR-223.
conclusionOverexpression of SIRT1 upregulated miR-223 expression, which attenuated the LPS-induced neutrophil activity and inflammatory response. The SIRT1/miR-223 signaling axis provides a potential therapeutic target for the clinical management of neonatal sepsis.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.