ArticleThe American journal of pathology2010
Hepatic fibrosis is enhanced and accompanied by robust oval cell activation after chronic carbon tetrachloride administration to Egr-1-deficient mice.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Altered AP-1, RUNX, and EGR chromatin dynamics drive human fibrotic lung disease.Annals of the rheumatic diseases · 2026Article
- A Shared EGR1-IL-32-Macrophage Polarisation Signature in Rheumatoid Arthritis and Metabolic Dysfunction-Associated Steatotic Liver Disease.Journal of inflammation research · 2026Article
- Regression of hepatic fibrosis in gamma-irradiated rats by mycophenolate mofetil: potential role of Egr-1.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Hepatic kinome atlas: An in-depth identification of kinase pathways in liver fibrosis of humans and rodents.Hepatology (Baltimore, Md.) · 2022Article
- Sex-Dependent Effects on Liver Inflammation and Gut Microbial Dysbiosis After Continuous Developmental Exposure to Trichloroethylene in Autoimmune-Prone Mice.Frontiers in pharmacology · 2020Article
- Isolation and Enrichment of Liver Progenitor Subsets Identified by a Novel Surface Marker Combination.Journal of visualized experiments : JoVE · 2017Article
- Elk-3 Contributes to the Progression of Liver Fibrosis by Regulating the Epithelial-Mesenchymal Transition.Gut and liver · 2017Article
- Role of early growth response 1 in liver metabolism and liver cancer.Hepatoma research · 2017Article
- Reproductive age-associated fibrosis in the stroma of the mammalian ovary.Reproduction (Cambridge, England) · 2016Article
- Egr-1 deficiency protects from renal inflammation and fibrosis.Journal of molecular medicine (Berlin, Germany) · 2016Article
- Moderate (2%, v/v) Ethanol Feeding Alters Hepatic Wound Healing after Acute Carbon Tetrachloride Exposure in Mice.Biomolecules · 2016Article
- Podoplanin discriminates distinct stromal cell populations and a novel progenitor subset in the liver.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Macrophage migration inhibitory factor is required for recruitment of scar-associated macrophages during liver fibrosis.Journal of leukocyte biology · 2015Article
- Constitutive Activation of the Nlrc4 Inflammasome Prevents Hepatic Fibrosis and Promotes Hepatic Regeneration after Partial Hepatectomy.Mediators of inflammation · 2015Article
- Toxicogenomic analysis reveals profibrogenic effects of trichloroethylene in autoimmune-mediated cholangitis in mice.Toxicological sciences : an official journal of the Society of Toxicology · 2014Article
- Modeling toxicodynamic effects of trichloroethylene on liver in mouse model of autoimmune hepatitis.Toxicology and applied pharmacology · 2014Article
- Peritumoral ductular reaction: a poor postoperative prognostic factor for hepatocellular carcinoma.BMC cancer · 2014Article
- Genetic resistance to liver fibrosis on A/J mouse chromosome 17.Alcoholism, clinical and experimental research · 2013Article
- Transcription factor EGR1 directs tendon differentiation and promotes tendon repair.The Journal of clinical investigation · 2013Article
- Kupffer cells in the liver.Comprehensive Physiology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The transcription factor early growth response (Egr)-1 regulates the expression of genes required for execution of the wound healing response. Multiple cycles of injury, coupled to incomplete wound healing, lead to fibrosis. Therefore, we hypothesized that Egr-1 is required for the development of hepatic fibrosis. To test this hypothesis, we exposed wild-type and egr-1(-/-) mice to acute or chronic carbon tetrachloride (CCl(4)). Acute CCl(4) exposure established a profibrotic milieu in the liver, including activation of hepatic stellate cells as well as expression of type 1 collagen genes and tissue inhibitor of matrix metalloproteinase 1 in both wild-type and egr-1(-/-) mice. This response was exacerbated in egr-1(-/-) mice. After chronic CCl(4) exposure, hepatic fibrosis was established in both genotypes; however, the fibrotic response was profoundly worsened in Egr-1-deficient mice. Importantly, enhanced fibrosis in egr-1(-/-) mice was accompanied by a robust activation of the oval cell response, suggesting more severe liver injury and/or reduced hepatocyte proliferation when compared with wild-type mice. Hepatic expression of genes indicative of oval cell activation, as well as the number of cells expressing A6, a mouse oval cell marker, was greater in egr-1(-/-) mice. Taken together, these data reveal novel roles for Egr-1 as a negative regulator of both CCl(4)-induced hepatic fibrosis and the oval cell response.
Indexed as
Identifiers
What OpenQuestion holds
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.