ReviewJournal of cellular and molecular medicine2025
STAT3 Facilitates Super Enhancer Formation to Promote Fibroblast-To-Myofibroblast Differentiation by the Analysis of ATAC-Seq, RNA-Seq and ChIP-Seq.
Review in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Beryllium Sulfate-Induced Cellular Senescence via the IL-6/STAT3 Pathway to Promote Pulmonary Fibrosis.Journal of applied toxicology : JAT · 2026Article
- circCACNA1D drives pulmonary fibrosis by regulating pyruvate kinase M2 dimer‑tetramer switching.International journal of molecular medicine · 2026Article
- Long non-coding RNA NPPA-AS1 acts as a potential novel biomarker and promotes atrial fibrillation progression via the miR-302e/TGFBR2 axis.Journal of thrombosis and thrombolysis · 2026Article
- The PPAR-gamma agonist pioglitazone alleviates bleomycin-induced lung fibrosis in male BALB/c mice.Multidisciplinary respiratory medicine · 2026Article
- Transcriptional factor ATF3 impairs KSHV lytic replication by suppressing the expression of viral bZIP protein K8.PLoS pathogens · 2026Article
- Mitochondrial PDHA1 acetylation orchestrates lactate-dependent epigenetic reprogramming to promote fibrosis via NUAK2.Cellular and molecular life sciences : CMLS · 2026Article
- Decoding macrophage heterogeneity in the pulmonary fibrosis lung cancer transition.Frontiers in immunology · 2026Review
- Stathmin-mediated autophagy drives the differentiation of dermal fibroblast into myofibroblast under TGFβ1 stimulation.Molecular biology reports · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
A cellular characteristic of IPF is the transformation of fibrosis into myofibroblasts. This study identifies several transcription factors-STAT3, FOXP1, JUNB, ATF3, FosL2, BATF, Fra2 and AP-1-that play crucial roles in promoting pulmonary fibrogenesis. They achieve this by facilitating the differentiation of fibroblasts into myofibroblasts, as analysed through ATAC-seq and RNA-seq. Additionally, STAT3 ChIP-seq showed that STAT3 is significantly concentrated in accessible chromatin regions, including introns and intergenic areas. H3K27ac ChIP-seq and Co-IP demonstrated that STAT3 plays a role in the formation of super enhancer (SE), which promotes gene expression. CUT&RUN-qPCR and the pGL3-SE dual-luciferase reporter system assays proved that STAT3 enhanced pGL3-SE activities by facilitating H3K27ac modification, leading to promoting the transcription of target genes including RUNX1, JUNB, JUN, SMAD6, COL3A1 and PTPN1. In summary, this study shows that STAT3 contributes to the formation of SEs that accelerate the differentiation of fibroblasts into myofibroblasts, leading to IPF. This insight enhances our understanding of STAT3-related SEs and offers potential therapeutic strategies for fibrotic diseases.
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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.