ArticleJournal of translational medicine2025
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Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
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
4 citing papers in PubMed.
- mExperimental and therapeutic medicine · 2026Review
- Integrative Genomic and Transcriptomic Insights into High-Altitude Adaptation in Changthangi Goats.Applied biochemistry and biotechnology · 2026Article
- AI-driven drug-target interaction prediction: current progress, challenges, and future roadmap for precision medicine.Journal of computer-aided molecular design · 2026Review
- Intelligent design of tumor microenvironment-responsive Adeno-associated virus vectors: overcoming delivery barriers and enabling precision therapy.Medical oncology (Northwood, London, England) · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
backgroundSilicosis is a severe and globally prevalent lung disease characterized by progressive pulmonary fibrosis. Recent studies suggested that N6-methyladenosine (m6A) modification is implicated in the pathogenesis of lung diseases. However, the function role of m6A modification in silicosis is still mostly unknown.
methodsSilica-exposed bronchial epithelial cell model and silicosis mice model were established to determine the role of m6A modification in silica-induced pulmonary fibrosis. Then, a series of experimental methods including dot blot, immunofluorescence, RIP assay, were performed to explore the underlying mechanisms of methyltransferase-like 3 (METTL3)-mediated Differentiated embryo-ehon-drocyte expressed gene1 (DEC1) m6A modification in epithelial-mesenchymal transition (EMT) process and pulmonary fibrosis. Finally, we used small interfering RNAs (siRNAs) and AAV6 vectors targeting METTL3 to investigate the effect of METTL3 in silica-induced pulmonary fibrosis.
resultsWe found that silica-induced EMT process was accompanied by the increased expression of DEC1. Mechanistically, DEC1 was identified as the downstream effector of METTL3. METTL3 directly recognized and bound to the m6A site on DEC1 mRNA, regulated DEC1 mRNA stability, leading to its post-transcriptional activation. DEC1 then activated PI3K/Akt signaling pathway, and played a critical role in silica-induced pulmonary fibrosis by promoting inflammation and EMT process. In particular, the EMT process and silica-induced pulmonary fibrosis were alleviated by siRNAs and AAV6 vectors targeting METTL3 in vitro and in vivo, respectively.
conclusionsThe m6A-mediated regulation of DEC1 overexpression may underlie the pathogenesis of silicosis, suggesting that modulation of METTL3 mediated DEC1 expression represents a promising prevention target.
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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.