ArticleJournal of advanced research2026
Long noncoding RNA Nron and its functional motif modulate macrophage-mediated inflammatory response.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Epigenetic Mechanisms in Sepsis-Induced Cardiomyopathy: From Pathophysiology to Therapeutic Targets.International journal of molecular sciences · 2026Review
- lncRNA-mRNA Co-expression Network Unveils Neutrophil Metabolic Reprogramming in Human Sepsis.Inflammation · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionNon-resolving macrophage-mediated inflammation is closely linked to the pathogenesis of systemic inflammatory response syndrome. Despite years of clinical trials attempting to mitigate the harmful effects of excessive inflammation, these efforts have largely been unsuccessful. Therefore, it is essential to develop novel therapeutic strategies.
objectiveTo explore the role of Nron in inflammatory diseases and evaluate the therapeutic effect.
methodsConditional knockout/knockin mice were used for a systematic evaluation of Nron function in lipopolysaccharide (LPS) or cecal ligation and puncture (CLP)-induced sepsis. Quantitative real-time PCR, western blot, luciferase reporter assay, and RNA-RNA interaction assay were performed to investigate mechanisms and identify functional motifs. An enhanced lipid nanoparticle (LNP) formulation was constructed for targeted macrophage delivery and therapy. Moreover, monocytes were obtained from blood of patients with sepsis for in vitro culture, and the serum for enzyme-linked immunosorbent assay (ELISA) detection. Data analysis was conducted using GraphPad Prism 8.
resultsConditional knockout of Nron in myeloid cells exacerbates LPS or CLP-induced sepsis, while the conditional transgenic mice exhibited a survival advantage with alleviated tissue inflammation and damage. Nron enhances sirtuin 1 (SIRT1) deacetylase activity via sponging miR-146a-3p/miR-16-1-3p in macrophages, thus regulating on nuclear factor kappa B (NF-κB) signaling by inhibiting p65 acetylation/phosphorylation directly or via HIF-1 signaling. The conserved functional motif of Nron (NCM2) has a longer half-life and LNP-NCM2 targeted to macrophages effectively alleviated sepsis in mice.
conclusionNron serves as a crucial negative regulator of excessive inflammatory responses, and its functional motifs can be used as a potential therapeutic agent for inflammatory diseases such as sepsis.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.