ArticleJournal of dental sciences2025
Hepcidin promotes oral ulcer healing via amphiregulin production in rats.
Article in Journal of dental sciences, 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.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background/purpose: Hepcidin is an antimicrobial peptide that regulates iron metabolism. Recently, hepcidin was reported to promote wound healing. However, the mechanism underlying hepcidin signaling in the oral mucosa remains unclear. In the present study, we examined the mechanism by which hepcidin accelerates healing in a rat model of oral ulcerative mucositis. Materials and methods: In male Wistar rats, 50 % acetic acid was applied to the labial fornix region of the inferior incisors to create a model of oral ulcerative mucositis. The ulcerative mucositis severity was evaluated using an oral mucositis score. Hepcidin expression, phosphorylation of the hepcidin receptor ferroportin and the levels of the epidermal growth factor amphiregulin were assessed using immunohistochemistry and western blotting. Hepcidin was applied to the oral mucosal region of rats with exacerbated oral ulcerative mucositis, which developed following acetic acid treatment after extraction of the submandibular and sublingual glands. Results: Two and five days after acetic acid treatment, hepcidin levels increased in the ulcerated region and saliva. Ferroportin in the ulcerated region was phosphorylated 2 days after acetic acid treatment. The expression and amount of amphiregulin in the ulcerated region increased on days 2 and 5. In exacerbated oral ulcerative mucositis rats, the oral ulcerative mucositis healing period was prolonged, and hepcidin and amphiregulin levels in the ulcerated region decreased. Daily hepcidin application to the ulcerated region shortened the healing period in exacerbated oral ulcerative mucositis rats. Conclusion: Oral ulcerative mucositis-induced increase in hepcidin promotes healing through the amphiregulin production of via ferroportin activation.
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.