ArticleThe American journal of pathology2013
Early growth response 3 (Egr-3) is induced by transforming growth factor-β and regulates fibrogenic responses.
Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 67 citations in OpenAlex.
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- Altered AP-1, RUNX, and EGR chromatin dynamics drive human fibrotic lung disease.Annals of the rheumatic diseases · 2026Article
- Conserved Transcriptional Circuits Regulate Cardiac Fibroblast-Mediated Fibrosis.Circulation research · 2026Article
- Integrative Single-Cell and Spatial Transcriptomics Identifies CRIP1Mediators of inflammation · 2026Article
- Variable steady inflammation and inflammatory responses in precision-cut lung slices from various IPF lung Regions.Respiratory research · 2025Article
- Comprehensive transcription factor perturbations recapitulate fibroblast transcriptional states.Nature genetics · 2025Article
- Seasonal Temperature Differentially Modulates the Immunotranscriptomic Performance in Atlantic Salmon Skin in Response to NaturalAnimals : an open access journal from MDPI · 2025Article
- Sirtuin 4 accelerates heart failure development by enhancing reactive oxygen species-mediated profibrotic transcriptional signaling.Journal of molecular and cellular cardiology plus · 2025Article
- Hepatic stellate cell single cell atlas reveals a highly similar activation process across liver disease aetiologies.JHEP reports : innovation in hepatology · 2025Article
- Single-cell analysis reveals the loss of FABP4-positive proliferating valvular endothelial cells relates to functional mitral regurgitation.BMC medicine · 2024Article
- Fibroblast-specific TGF-β signaling mediates cardiac dysfunction, fibrosis, and hypertrophy in obese diabetic mice.Cardiovascular research · 2024Article
- flt1 inactivation promotes zebrafish cardiac regeneration by enhancing endothelial activity and limiting the fibrotic response.Development (Cambridge, England) · 2024Article
- DNA Methylation Profiling in Genetically Selected Clarias magur (Hamilton, 1822) Provides Insights into the Epigenetic Regulation of Growth and Development.Marine biotechnology (New York, N.Y.) · 2024Article
- A statistical approach for identifying single nucleotide variants that affect transcription factor binding.iScience · 2024Article
- Article
- Loss of SLC27A5 Activates Hepatic Stellate Cells and Promotes Liver Fibrosis via Unconjugated Cholic Acid.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Intrafusal-fiber LRP4 for muscle spindle formation and maintenance in adult and aged animals.Nature communications · 2023Article
- Macromolecular crowding regulates matrix composition and gene expression in human gingival fibroblast cultures.Scientific reports · 2023Article
- The circular RNA circNlgnmediates doxorubicin-inducedcardiac remodeling and fibrosis.Molecular therapy. Nucleic acids · 2022Article
- Biological substrate modification suppresses ventricular arrhythmias in a porcine model of chronic ischaemic cardiomyopathy.European heart journal · 2022Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Members of the early growth response (Egr) gene family of transcription factors have nonredundant biological functions. Although Egr-3 is implicated primarily in neuromuscular development and immunity, its regulation and role in tissue repair and fibrosis has not been studied. We now show that in normal skin fibroblasts, Egr-3 was potently induced by transforming growth factor-β via canonical Smad3. Moreover, transient Egr-3 overexpression was sufficient to stimulate fibrotic gene expression, whereas deletion of Egr-3 resulted in substantially attenuated transforming growth factor-β responses. Genome-wide expression profiling in fibroblasts showed that genes associated with tissue remodeling and wound healing were prominently up-regulated by Egr-3. Notably, <5% of fibroblast genes regulated by Egr-1 or Egr-2 were found to be coregulated by Egr-3, revealing substantial functional divergence among these Egr family members. In a mouse model of scleroderma, development of dermal fibrosis was accompanied by accumulation of Egr-3-positive myofibroblasts in the lesional tissue. Moreover, skin biopsy samples from patients with scleroderma showed elevated Egr-3 levels in the dermis, and Egr-3 mRNA levels correlated with the extent of skin involvement. These results provide the first evidence that Egr-3, a functionally distinct member of the Egr family with potent effects on inflammation and immunity, is up-regulated in scleroderma and is necessary and sufficient for profibrotic responses, suggesting important and distinct roles in the pathogenesis of fibrosis.
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