ReviewNaunyn-Schmiedeberg's archives of pharmacology2026
Neuroimmune pharmacotherapy across the skin-brain axis: mechanisms, therapeutic targets, and AI-enabled precision approaches.
Review in Naunyn-Schmiedeberg's archives of pharmacology, 2026. 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The skin-brain axis is a bidirectional neuroimmune network linking cutaneous inflammation with central neuroinflammation, stress signaling, and behavioral disturbances. This review summarizes the mechanisms underlying skin-brain communication and evaluates current and emerging pharmacological strategies targeting this axis in inflammatory skin disorders. We synthesized contemporary experimental, translational, and clinical evidence on neuroimmune signaling across the skin-brain axis, with emphasis on sensory neuron-immune cell interactions, neurogenic inflammation, glial activation, pharmacological targets, biomarkers, disease models, and artificial intelligence (AI)-enabled precision approaches. Current evidence suggests that chronic cutaneous inflammation may promote central neuroimmune activation through neuropeptides, cytokines, and stress-responsive pathways. Central stress signaling can, in turn, exacerbate skin disease. Substance P, calcitonin gene-related peptide, transient receptor potential channels, microglia, and astrocytes emerge as key mediators linking peripheral inflammation to altered neuroplasticity and affective symptoms. Therapeutic approaches including biologics, Janus kinase and phosphodiesterase-4 inhibitors, neuromodulators, and transient receptor potential antagonists show promise in reducing pruritus and neuropsychiatric comorbidity. However, pharmacodynamic variability and incomplete response remain important limitations. Biomarkers, multi-omic profiling, and advanced preclinical models may improve translational evaluation, while AI tools may support biomarker discovery, digital phenotyping, and individualized treatment selection. The skin-brain axis represents a pharmacologically actionable framework for inflammatory skin disease. Integrated strategies addressing peripheral inflammation, central neuroimmune dysregulation, and psychosocial burden may improve precision pharmacotherapy and clinical outcomes.
Indexed as
Identifiers
42696144What 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.