ArticleInflammation2026
MAGL Inhibition Relieves Psoriasiform Inflammation and Pruritus Via Modulation of ALOX12-12-HETE Axis in Mice.
Article in Inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- Skin on Drugs: Psychotropic Compounds in Cutaneous Biology.International journal of molecular sciences · 2026Review
- Integrated lipidomic and transcriptomic profiling of imiquimod-induced psoriasiform dermatitis.Frontiers in cell and developmental biology · 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
10 authors.
Funding
Abstract
The endogenous cannabinoid system, comprising endocannabinoids, cannabinoid receptors, and enzymes responsible for synthesis and degradation of endocannabinoids, is integral to the regulation of skin inflammation. However, the precise contributions of cannabinoid-metabolizing enzymes including fatty acid amide hydrolase and monoacylglycerol lipase (MAGL) remain poorly defined in psoriatic pathogenesis. In this study, we demonstrated the significant MAGL upregulation in psoriatic lesions and established that pharmacological inhibition of MAGL markedly reduced psoriasiform inflammation and pruritus in imiquimod-challenged C57BL/6 mice. Mechanically, inhibition of MAGL decreased the expression of 12-lipoxygenase (ALOX12), subsequently reducing the synthesis of 12-hydroxyeicosatetraenoic acid (12-HETE), which is the principal metabolite of ALOX12. Importantly, these effects were reversed by cannabinoid receptor 2 (CB2R) antagonism or knockout, establishing a signaling axis in which MAGL inhibition activates CB2R to suppress ALOX12. Collectively, our findings identified MAGL as a potentially targetable nexus in psoriasiform inflammation and itch.
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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 OpenQuestion graph.