ArticleCentral-European journal of immunology2025
p65 enhanced METTL3-mediated m
Article in Central-European journal of immunology, 2025. 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Sepsis-associated encephalopathy (SAE) is a complication posing a significant risk to patient health and survival. Microglial polarization and inflammation are key to the pathological progression of SAE. The p65 subunit is a component of the nuclear factor- Material and methods: Human microglial HMC3 cells were treated with lipopolysaccharide (LPS). Cell viability was measured using a CCK-8 kit. Proinflammatory cytokine levels were evaluated using an ELISA assay. qRT-PCR or western blot assays were used to estimate mRNA or protein levels. The proportion of microglial M1 polarization was assessed using flow cytometry. The m6A-modified high mobility group box 1 (HMGB1) levels were analyzed using MeRIP-qPCR. Dual-luciferase reporter, chromatin immunoprecipitation (ChIP), and RNA immunoprecipitation (RIP) assays were conducted to validate the interactions between p65 and methyltransferase-like 3 (METTL3) or between METTL3 and HMGB1. Results: LPS promoted microglial M1 polarization and enhanced p65, METTL3, and HMGB1 expression. Further, the inhibition of p65 ameliorated the LPS-induced M1 microglial polarization. p65 promotes HMGB1 m6A methylation by transcriptionally activating METTL3. Under LPS treatment, p65 enhances microglial M1 polarization via METTL3 activation. METTL3 aggravates LPS-induced microglial M1 polarization by positively regulating HMGB1 m6A modification. Conclusions: p65 increases LPS-induced M1 polarization by promoting METTL3-mediated m6A modification of HMGB1 in HMC3 cells.
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.