ArticleImmunoTargets and therapy2025
Regulation of Histone Acetylation During Inflammation Resolution.
Article in ImmunoTargets and therapy, 2025. 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.
- Modulation and Reprogramming of Adipose Tissue Macrophages in Obesity.Biomolecules · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Inflammatory resolution is an active and coordinated process. Histone acetylation represents the primary epigenetic alteration associated with inflammatory diseases. However, the precise role of histone acetylation in the resolution of inflammation remains poorly understood. Methods: Lipopolysaccharide (1 µg/mL, 10 ng/mL) and Results: Our analysis reveals that histone acetylation and acetyl CoA are temporally regulated during the inflammatory response. A low-dose challenge results in heightened histone acetylation and reduced acetyl CoA. Metabolic repatterning during the inflammatory response promotes the generation of acetyl CoA and histone acetylation. Furthermore, the overexpression of histone acetylation enhances the production of anti-inflammatory lipid mediators, particularly the specialized pro-resolving lipid mediators (SPMs). Conclusion: These findings illustrate that histone acetylation is not only temporally and differentially regulated during inflammatory responses but also interacts with metabolic reprogramming to promote the production of SPMs, thereby facilitating inflammation resolution.
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.