ArticleScientific reports2025
Effects of Slit2 on hypertrophic scar formation: an in vitro study in fibroblasts.
Article in Scientific reports, 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
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
2 citing papers in PubMed.
- The LncRNA GAS5/miR-205 ceRNA axis regulates fibroblast activation and may contribute to hypertrophic scarring.Molecular biology reports · 2026Article
- Reprogramming the wound microenvironment: identity remodeling strategies for fibroblasts, keratinocytes, and macrophages.Frontiers in immunology · 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
7 authors.
Funding
Abstract
Hypertrophic scarring (HTS) is a common complication of burns and has been associated with Slit2 protein. Slit2 plays various physiological and pathological roles in some body organs and tumors. However, its role in HTS development remains poorly understood. Therefore, this study investigated the involvement of intracellular and exogenous Slit2 in hypertrophic scar formation in vitro. Human normal fibroblasts (HNFs) and hypertrophic scar fibroblasts (HTSFs) were isolated from normal skin and hypertrophic scar tissues, respectively. Immunohistochemistry was conducted, and molecular expressions were detected by real-time polymerase chain reaction and western blotting. Cell proliferation and mobility were assessed. The results showed that Slit2 and Robo1 expressions were higher in the dermis of HTS tissues and HTSFs than in normal skin and HNFs. Downregulation of Slit2 expression by siRNA transfection reduced the expression of alpha-smooth muscle actin (α-SMA) and extracellular matrix in HTSFs. Additionally, treatment with recombinant Slit2 protein enhanced cell proliferation, expression of α-SMA, ECM, vimentin, N-cadherin, and migration by inducing the phosphorylation of both SMAD and non-SMAD signaling in HNFs. These findings highlight the active role of Slit2 in HTS formation, offer new insights into HTS pathology, and suggest Slit2 as a potential therapeutic target for post-burn hypertrophic scarring.
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.