ArticleArchives of dermatological research2025
The transcription factor TCF4 regulates the miR-494-3p/THBS1 axis in the fibrosis of pathologic scars.
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. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
backgroundThe fibrosis of pathologic scar (PS) is formed by the excessive deposition of extracellular matrix, resulting in an abnormal scar. Recent clinical tests have indicated that the regulation of PS fibroblast cells (PSF cells) proliferation can serve as an intervention measure for PS. Our work aimed to elucidate the specific mechanism of action of TCF4 on the progression of PS fibrosis.
methodsOur study used qRT-PCR and Western blot to search for the expression of key proteins in PS clinical samples and cells. Transwell, CCK-8, and wound scratch assays were employed to analyze the proliferation and migration of PSF cells. CHIP, dual-luciferase reporter experiments, and bio-informatics analysis were used to analyze the interactions between molecules.
resultsThe analysis of PS clinical samples confirmed a positive correlation between TCF4 and miR-494-3p. This regulatory mechanism was related to the progression of PS. We verified that the overexpression of miR-494-3p or the knockdown of THBS1 both suppressed the proliferation and migration of PSF cells. Furthermore, we also confirmed the binding relationships between TCF4, miR-494-3p, and THBS1. Simultaneously, we verified the existence of the TCF4/miR-494-3p/THBS1 regulatory network in PS. This regulatory process affects the development of PS fibrosis.
conclusionOur study results indicate that TCF4, miR-494-3p, and THBS1 are abnormally expressed in PS. TCF4 increases the proliferation and migration ability of PSF cells through the miR-494-3p/THBS1 signaling pathway, which promotes the fibrosis of PS.
Indexed as
Identifiers
39786568What 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.