ReviewMatrix biology : journal of the International Society for Matrix Biology2011
Early growth response transcription factors: key mediators of fibrosis and novel targets for anti-fibrotic therapy.
Review in Matrix biology : journal of the International Society for Matrix Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 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
74 citing papers in PubMed, 128 citations in OpenAlex.
- Transcriptomic Profiling Identifies Disease-Specific miRNA-mRNA Regulatory Networks in Systemic Sclerosis.Biomolecules · 2026Article
- Centrosomal protein 72 deficiency exacerbates liver fibrosis induced by Schistosoma japonicum infection.Parasites & vectors · 2026Article
- Simultaneous inhibition of ID1 and ID3 mitigates fibroblast activation via cell cycle and MEK/ERK pathways in pulmonary fibrosis.Theranostics · 2026Article
- Regression of hepatic fibrosis in gamma-irradiated rats by mycophenolate mofetil: potential role of Egr-1.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Identification of epigenetic regulators of fibrotic transformation in cardiac fibroblasts through bulk and single-cell CRISPR screens.Nature communications · 2025Article
- Role of Growth Factors in the Pathogenesis of Systemic-Sclerosis-Associated Fibrosis.International journal of molecular sciences · 2025Review
- Sirtuin 4 accelerates heart failure development by enhancing reactive oxygen species-mediated profibrotic transcriptional signaling.Journal of molecular and cellular cardiology plus · 2025Article
- Shared roles of immune and stromal cells in the pathogenesis of human bronchiolitis obliterans syndrome.JCI insight · 2025Article
- Heart Rate Mystery Unveiled: Sex Differences in Human Sinoatrial Node Genes and Female Tachycardia.Circulation. Arrhythmia and electrophysiology · 2025Article
- Spaceflight causes strain-dependent gene expression changes in the kidneys of mice.NPJ microgravity · 2025Article
- Article
- Heme oxygenase 1-mediated ferroptosis in Kupffer cells initiates liver injury during heat stroke.Acta pharmaceutica Sinica. B · 2024Article
- Article
- Expression profiling by high-throughput sequencing reveals GADD45, SMAD7, EGR-1 and HOXA3 activation in Myostatin (MSTN) and GDF11 treated myoblasts.Genetics and molecular biology · 2024Article
- Early growth response-1, a dynamic conduit in cardiovascular disease.Frontiers in cardiovascular medicine · 2024Review
- Identifying health risk determinants and molecular targets in patients with idiopathic pulmonary fibrosis via combined differential and weighted gene co-expression analysis.Frontiers in genetics · 2024Article
- HK-2 cell response to TGF-β highly depends on cell culture medium formulations.Histochemistry and cell biology · 2024Article
- IRX2 regulates angiotensin II-induced cardiac fibrosis by transcriptionally activating EGR1 in male mice.Nature communications · 2023Article
- A CRISPR/Cas9-engineered mouse carrying a conditional knockout allele for the early growth response-1 transcription factor.Genesis (New York, N.Y. : 2000) · 2023Article
- Regulation of chromatin organization during animal regeneration.Cell regeneration (London, England) · 2023Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Fibrosis is a deregulated and ultimately defective form of tissue repair that underlies a large number of chronic human diseases, as well as obesity and aging. The pathogenesis of fibrosis involves multiple cell types and extracellular signals, of which transforming growth factor-ß (TGF-ß) is pre-eminent. The prevalence of fibrosis is rising worldwide, and to date no agents has shown clinical efficacy in the attenuating or reversing the process. Recent studies implicate the immediate-early response transcription factor Egr-1 in the pathogenesis of fibrosis. Egr-1 couples acute changes in the cellular environment to sustained alterations in gene expression, and mediates a broad spectrum of biological responses to injury and stress. In contrast to other ligand-activated transcription factors such as NF-κB, c-jun and Smad2/3 that undergo post-translational modification such as phosphorylation and nuclear translocation, Egr-1 activity is regulated via its biosynthesis. Aberrant Egr-1 expression or activity is implicated in cancer, inflammation, atherosclerosis, and ischemic injury and recent studies now indicate an important role for Egr-1 in TGF-ß-dependent profibrotic responses. Fibrosis in various animal models and human diseases such as scleroderma (SSc) and idiopathic pulmonary fibrosis (IPF) is accompanied by aberrant Egr-1 expression. Moreover Egr-1 appears to be required for physiologic and pathological connective tissue remodeling, and Egr-1-null mice are protected from fibrosis. As a novel profibrotic mediator, Egr-1 thus appears to be a promising potential target for the development of anti-fibrotic therapies.
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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.