ArticleArchives of dermatological research2025
Platelet-rich fibrin attenuates inflammation and fibrosis in vulvar lichen sclerosus via the TGF-β/SMAD3 pathway.
Article in Archives of dermatological research, 2025. 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
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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.
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Who cites it
2 citing papers in PubMed.
- Silk fibroin hydrogel with recombinant silk fibroin/NT3 protein enhances wound healing by promoting type III collagen synthesis and hair follicle regeneration in skin injury.Materials today. Bio · 2025Article
- First Report of Successful Treatment of Erosive Vulvovaginal Lichen Planus with Platelet-Rich Fibrin: A Case Report and Comprehensive Literature Review.Case reports in dermatologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Vulvar lichen sclerosus (VLS) is a chronic, inflammatory, and progressive skin disease mainly involved in the anogenital area. Platelet-rich fibrin (PRF) is a fibrin adhesive-concentrated platelet-rich plasma (PRP) used for tissue repair and angiogenesis. In this study, we explored the effects of PRF on VLS patients, further to utilize the established VLS animal model, to confirm the therapeutic effect of PRF and regulation on the TGF-β/SMAD3 pathway. Among the 46 VLS patients included in the analysis, injectable RPF (i-PRF) treatment improved the symptoms of VLS. The immunohistochemical analysis showed that i-PRF decreased the local blurring of the dermal-epidermal boundary and increased the number of basal keratinocytes. I-PRF increased positive PGD9.5, CD34, and Melan A cell numbers, and decreases positive IL-17 and INF-γ cell numbers in VLS tissues. In the VLS rat model, i-PRF reduced inflammatory factors IL-17 and INF-γ via inhibition of NF-κB and increased CD31 and VEGF expression in external genital tissue. The i-PRF decreases fibronectin and collagen-I by inhibiting TGF-β/SMAD3 in VLS, which is the main factor that triggers inflammation and fibrosis of the external genital skin.
Indexed as
Identifiers
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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.