ArticleJournal of pain research2025
GPER Enhances Chronic Burn Pain via PKC-Mediated Mu-Opioid Receptor Phosphorylation in the Rostral Ventromedial Medulla.
Article in Journal of pain research, 2025. 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.
- 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Chronic pain following burn injury represents a formidable challenge in analgesic management, as the complex interplay and dynamic nature of multiple neural mechanisms underlying abnormal hyperalgesia renders its resolution exceptionally problematic. The G protein-coupled estrogen receptor (GPER) located within the rostral ventromedial medulla (RVM) has been recognized as a critical element in regulating descending pain signal transmission throughout the brain. Nevertheless, the precise underlying mechanisms remain insufficiently elucidated. This investigation examined GPER function in chronic pain modulation and its role in pain rehabilitation. Methods and Results: A murine model of burn injury-induced chronic pain was employed, wherein nociceptive paw withdrawal reflexes to both thermal and mechanical stimuli were evaluated. In contrast to mice exhibiting pain resolution, a subset displaying sustained or stimulus-evoked reductions in pain threshold developed a persistent pain phenotype. Notably, prolonged hyperalgesia post-burn injury was associated with GPER activation. GPER-immunoreactive neurons were found to be co-localized with activated protein kinase C (PKC) and μ-opioid receptor (MOR) in murine tissues. Moreover, in mice with persistent pain, phosphorylation of MOR-facilitated by activated PKC rather than GRK 2/3-was implicated in GPER-dependent nociceptive allodynia, a process effectively reversed by selective PKC inhibition. In these animals, attenuation of PKC activation significantly elevated the pain threshold by inhibiting MOR phosphorylation. Conclusion: These findings highlight the involvement of GPER-dependent PKC-mediated MOR phosphorylation in RVM during postoperative chronic pain development. These insights may contribute to an enhanced understanding of chronic pain's fundamental mechanisms and suggest potential preventive approaches for analgesic interventions.
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.