ArticleMediators of inflammation2026
SNHG5 Exacerbates Sepsis-Induced Inflammatory Injury in Coronary Artery Endothelial Cells by Regulating METAP2-Mediated IL-8 Secretion.
Article in Mediators of inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- SNHG5 Exacerbates Sepsis-Induced Inflammatory Injury in Coronary Artery Endothelial Cells by Regulating METAP2-Mediated IL-8 Secretion.Mediators of 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Long noncoding RNAs (lncRNAs) are involved in regulating inflammatory responses in sepsis. This study aimed to investigate the potential roles of lncRNA SNHG5 in the pathogenesis of sepsis-induced coronary artery injury. Methods: Cecal ligation and puncture were used to establish a sepsis mouse model. Serum and coronary artery tissues were collected to assess inflammatory markers and lncRNA expression using enzyme-linked immunosorbent assay (ELISA) and real-time quantitative polymerase chain reaction (qPCR). In vitro, mouse aortic endothelial cells were exposed to septic serum. The SNHG5/miR-377-3p/methionyl aminopeptidase 2 (METAP2) axis was investigated using dual-luciferase reporter gene experiments. Loss-of-function, gain-of-function, and rescue assays were performed to elucidate the functions of these genes in sepsis. Results: Septic mice exhibited elevated systemic tumor necrosis factor alpha and interleukin (IL)-6 levels, as well as dysregulated endothelial markers (eNOS downregulation and ET-1 upregulation). Among the inflammation-related lncRNAs, SNHG5 was the most significantly upregulated in septic coronary arteries and serum. Bioinformatic and experimental analyses revealed that SNHG5 acts as a competitive endogenous RNA (ceRNA) for miR-377-3p, thereby upregulating (METAP2). Silencing SNHG5 or METAP2 reduced IL-8 secretion and endothelial apoptosis; these effects were reversed by miR-377-3p inhibition. Conversely, METAP2 overexpression increased IL-8 secretion and apoptosis, which were attenuated by miR-377-3p mimics. Conclusion: We identified the SNHG5/miR-377-3p/METAP2 axis as a novel regulatory pathway in sepsis-induced endothelial inflammation and apoptosis. SNHG5 promotes METAP2 expression by sponging miR-377-3p, leading to increased IL-8 secretion and endothelial dysfunction. These findings provide new insights into lncRNA-mediated mechanisms in 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.