ArticleJournal of molecular histology2025
METTL3 promotes the hypertrophic scar fibrosis via m6A RNA methylation of GRAMD1B mRNA.
Article in Journal of molecular histology, 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
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Who cites it
2 citing papers in PubMed.
- Exploring the Complexities of TGF-β Signaling in Keloids: Beyond the Classical Smad Pathway.International journal of molecular sciences · 2026Review
- The Central Role of m6A as Epigenetic Regulator in Metabolic Disorders of Therapeutic Potential and Clinical Implications.Molecular neurobiology · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Hypertrophic scarring (HS) is a common fibrotic disorder characterized by excessive extracellular matrix deposition and fibroblast proliferation. N6-methyladenosine (m6A) RNA methylation, mediated by METTL3, has emerged as a critical regulator of gene expression and cellular processes. This study investigates the role of METTL3-mediated m6A methylation in hypertrophic scar fibrosis. We found that METTL3 expression and m6A RNA methylation levels were significantly elevated in human hypertrophic scar tissues and TGF-β1-induced human dermal fibroblasts. Silencing METTL3 reduced m6A methylation, impaired fibroblast proliferation, and decreased the mRNA and protein expression of fibrotic markers (ACTA2, Col1a1, Col3a1, and CTGF). Bioinformatics analysis identified GRAMD1B as a key differentially expressed gene in HS tissues. METTL3-mediated m6A methylation enhanced GRAMD1B mRNA stability, promoting its expression. These findings suggest that METTL3 contributes to hypertrophic scar fibrosis by regulating m6A methylation of GRAMD1B mRNA, highlighting METTL3 as a potential therapeutic target for fibrotic disorders.
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.