ReviewFrontiers in immunology2026
Immunometabolic reprogramming in rheumatoid arthritis: the epitranscriptomic role of N6-methyladenosine in innate and adaptive immunity.
Review in Frontiers in immunology, 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.
- FTO in Bone Diseases: Functions, Mechanisms and Therapeutic Potential.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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N6-methyladenosine (m6A) methylation is the most common intramolecular modification in eukaryotic mRNA; its dynamic regulation depends on "writers" (methyltransferases: METTL3/METTL14/WTAP/VIRMA), "erasers" (demethylases: FTO/ALKBH5), and "readers" (binding proteins: YTHDF/YTHDC/IGF2BP families), thereby regulating RNA splicing, nuclear export, translation, and degradation. In rheumatoid arthritis (RA), this epigenetic network is severely disrupted: abnormal expression of writers leads to post-transcriptional activation of pro-inflammatory genes, while an imbalance in erasers compromises the stability of mRNAs encoding key signaling molecules. Together, these factors promote abnormal differentiation of immune cells, invasive proliferation of fibroblast-like synovial cells, and cartilage erosion. At the same time, hypoxia, inflammatory cytokines, and metabolic stress present in the joint microenvironment of RA induce cellular metabolic reprogramming, characterized by a shift toward aerobic glycolysis (Warburg effect), a reorganization of lipid synthesis and oxidation pathways, and an increase in glutamine uptake and catabolism; these changes all contribute to accelerating disease progression. Recent data have revealed a foundational integration between m6A modification and metabolic reprogramming: m6A regulators directly reshape the metabolic network by targeting transcripts encoding the glycolysis-limiting enzyme (HK2), key molecules in lipid metabolism (FASN/CPT1), and amino acid transporters (SLC1A5), thereby coordinating immune inflammation and tissue destruction in RA. This review elucidates the regulatory role of m6A methylation in the metabolic reprogramming of RA and explains how writers, erasers, and readers influence disease progression by participating in glycolysis, lipid metabolism, and glutamine metabolism. By focusing on the central question of whether m6A modification is the root cause of metabolic reprogramming in the pathogenesis of RA, we have integrated existing data to define the "m6A-metabolism-immunity" regulatory axis and identified potential therapeutic strategies targeting this association.
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.