ArticleAJOG global reports2025
TGF-β drives myofibroblast activation and inflammatory mediator production in vulvar lichen sclerosus.
Article in AJOG global reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
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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
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Molecular Mechanisms in the Etiopathology of Lichen Sclerosus: A Systematic Review.International journal of molecular sciences · 2026Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Vulvar lichen sclerosus (VLS) is a chronic inflammatory skin condition characterized by whitening of the external genitalia, debilitating pruritus (itching), and pain. As disease advances, loss of labia, burying of vulvar anatomy (ie, clitoris, urethra, vaginal opening), and vulvar cancer can occur, yet mechanistic understanding of these events remains limited. VLS lesions appear visibly similar to scars and are frequently referred to as such. Therefore, we investigated the role of fibrosis in the VLS disease mechanism with the goal of identifying targets for new therapeutic and diagnostic strategies. Study design: 6-mm biopsies were collected from 8 participants with VLS from regions of the vulva visibly affected by lichen sclerosus ("scarred") and adjacent unaffected areas ("unscarred"), allowing each patient to serve as their own control thus diminishing biological noise. Specimens were also used to establish fibroblast strains, and cells were stimulated with TGF-β to assess fibroblast-to-myofibroblast transitions, extracellular matrix (ECM) production, and inflammatory responses in scarred versus unscarred areas. Results: Fibroblasts from scarred areas expressed higher levels of cytoskeletal proteins (alpha-smooth muscle actin) and inflammatory mediators (interleukin 6, prostaglandin E2) upon TGF-β stimulation compared to their unscarred counterparts. Treatment with SB-431542, a TGF-β receptor inhibitor, quelled these responses ( Conclusion: TGF-β activates myofibroblasts and exacerbates inflammation in VLS cells from scarred areas. However, fibroblasts from both scarred and unscarred areas show similarities in morphology and ECM production, suggesting molecular changes may occur in VLS skin before visible changes are detected, which could lead to new diagnostic strategies to treat disease before irreversible architectural changes occur.
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