ArticleJournal of biomedical science2026
OPRM1/MRGPRX1 heterodimers drive opioid-induced itch through a peripheral mechanism.
Article in Journal of biomedical science, 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.
- Endosomal MrGPRX1 signaling sensitizes TRPV1 to enhance itch.Frontiers in molecular neuroscience · 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
6 authors.
Funding
Abstract
backgroundOpioid-induced itch is a common and distressing side effect of opioid analgesics, yet its underlying mechanisms remain poorly understood. While central µ-opioid receptor (OPRM1) signaling has been implicated, emerging evidence suggests that peripheral mechanisms also contribute, although their specific roles have not been clearly defined.
methodsWe investigated the interaction between OPRM1 and the itch-specific receptor MRGPRX1 in sensory neurons using bimolecular fluorescence complementation (BiFC), calcium and cAMP imaging, siRNA knockdown, and pharmacological inhibition assays. Behavioral assays in mice were conducted to assess scratching responses. We also employed immunohistochemistry, RT-qPCR, and ELISA to evaluate gene and protein expression levels in dorsal root ganglia (DRG) and skin tissues, including a mouse model of atopic dermatitis (AD).
resultsOPRM1 formed heterodimers with MRGPRX1 in HEK293T cells and sensory neurons, triggering a signaling switch from Gα
conclusionsOur findings identify a novel peripheral mechanism of opioid-induced itch mediated by OPRM1/MRGPRX1 heterodimers in sensory neurons. This receptor complex promotes calcium signaling and itch behavior, distinct from central or mast cell-dependent pathways. Targeting this heterodimer may offer new therapeutic strategies to alleviate opioid-induced itch without impairing analgesia.
Indexed as
Identifiers
What 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.