ArticleCells2025
Type V Collagen as a Critical Regulator of Fibrillar Matrix Remodeling in a Murine Model of Systemic Sclerosis.
Article in Cells, 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.
- Beyond Structure: The Dynamic Role of the Extracellular Matrix Components in Immune Evasion.Cancer communications (London, England) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
Abstract
Type V collagen (Col V) has been implicated in the development of fibrosis in systemic sclerosis (SSc). In this study, we aimed to investigate the role of Col V in fibrillar matrix remodeling and fibroblast differentiation using an experimental SSc model. Skin fibroblasts from healthy C57BL/6 mice were stimulated in vitro with 25 and 50 μg of Col V to assess fibrillar collagen expression. An SSc model was induced in C57BL/6 mice by immunization with Col V emulsified in Freund's adjuvant (IMU-COLV), with animals assigned to 15-, 30-, and 45-day IMU-COLV or control groups. In vitro, Col V stimulation caused a dose-dependent increase in myofibroblast markers (α-SMA, Col I, and Col V) and altered fibrillar collagen structure. Immunofluorescence revealed thickened Col V and Col III fibrils around myofibroblasts and the formation of a spiderweb-like matrix. In vivo, fibrosis progressed over time, characterized by increased myofibroblast accumulation and elevated Col I and Col V levels. Histological analysis revealed fibrillar disorganization and aggregated collagen fibers resembling early-stage human SSc. These findings suggest that enhanced Col V synthesis disrupts the fibrillar matrix, promoting myofibroblast differentiation and collagen deposition, which are hallmarks of SSc-related fibrosis.
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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.