ReviewFrontiers in pharmacology2026
Fatty acid-related immune network in psoriasis: metabolic regulation of innate and adaptive immunity.
Review in Frontiers in pharmacology, 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.
- Programming the tumor microenvironment through microbiome-driven mechanisms.Frontiers in cellular and infection microbiology · 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Psoriasis is a chronic inflammatory skin disorder driven by dysregulation of the Treg/Th17 axis, where enhanced Th17 activity promotes keratinocyte proliferation and inflammation, while impaired Treg function exacerbates immune dysregulation. Emerging evidence highlights peroxisome proliferator-activated receptor γ (PPARγ) as a key regulator of fatty acid oxidation (FAO), a metabolic pathway critical for Treg differentiation and function. PPARγ activation enhances FAO via upregulation of CD36, CPT1, and AMPK signaling, while suppressing glycolysis, thereby skewing the Treg/Th17 balance toward immune tolerance. Concurrently, short-chain fatty acids (SCFAs), microbial metabolites with immunomodulatory properties. ameliorate psoriatic inflammation by promoting Treg expansion, inhibiting Th17 polarization, and modulating innate immune cells (neutrophils, dendritic cells, and macrophages). SCFAs exert their effects through receptor-dependent signaling and epigenetic mechanisms (HDAC inhibition), while derivative compounds and probiotic interventions enhance therapeutic potential. This review summarizes mechanistic insights into PPARγ-driven FAO and SCFA-mediated immunomodulation, proposing novel metabolic and microbiome-targeted strategies for psoriasis treatment.
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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.