ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Depletion of p75NTR in Schwann Cells Driven by Inflammation Mediates Cutaneous Pain in Psoriasis.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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
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
2 citing papers in PubMed.
- LCN2-Driven Fibroblast Ferroptosis-Associated Injury Promotes Keratinocyte Proliferation via Lipid Peroxidation Signaling in Psoriasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Article
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
Skin pain is a common but poorly understood symptom of psoriasis, affecting only a subset of patients. Using imiquimod and interleukin-17A-induced psoriasiform mouse models that exhibited pain-like behaviors, we found that nerve growth factor (NGF) levels were elevated in lesional skin, activating TrkA signaling in dorsal root ganglion neurons and promoting Schwann-cell hypertrophy. Normally, Schwann cells (SCs) limit NGF signaling in cutaneous peripheral nerves through the p75NTR receptor. However, inflammation driven by interleukin-17A increased non-muscle myosin II activity and elevated NGF levels, leading to the internalization and degradation of p75NTR. The resulting depletion of p75NTR caused local NGF accumulation, excessive TrkA activation, and heightened pain sensitivity. These findings reveal that psoriatic inflammation converts SCs from protective buffers into drivers of pain, offering a mechanistic explanation for why only some patients experience cutaneous pain in psoriasis.
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.