ArticleDigestive diseases and sciences2008
Pathophysiological characteristics of dimethylnitrosamine-induced liver fibrosis in acute and chronic injury models: a possible contribution of KLF5 to fibrogenic responses.
Article in Digestive diseases and sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Regulatory roles and translational potential of the Kruppel-like factor family in liver disease.iLIVER · 2026Review
- A New Hypothetical Concept in Metabolic Understanding of Cardiac Fibrosis: Glycolysis Combined with TGF-β and KLF5 Signaling.International journal of molecular sciences · 2022Review
- Promoting roles of KLF5 in myocardial infarction in mice involving microRNA-27a suppression and the following GFPT2/TGF-β/Smad2/3 axis activation.Cell cycle (Georgetown, Tex.) · 2021Article
- Roles of Krüppel-like factor 5 in kidney disease.Journal of cellular and molecular medicine · 2021Review
- Pioglitazone protects blood vessels through inhibition of the apelin signaling pathway by promoting KLF4 expression in rat models of T2DM.Bioscience reports · 2019Article
- SP and KLF Transcription Factors in Digestive Physiology and Diseases.Gastroenterology · 2017Review
- Alleviation of Dimethylnitrosamine-Induced Liver Injury and Fibrosis by Supplementation of Anabasis articulata Extract in Rats.Indian journal of clinical biochemistry : IJCB · 2014Article
- Anchoring hepatic gene expression with development of fibrosis and neoplasia in a toxicant-induced fish model of liver injury.Toxicologic pathology · 2013Article
- Essential role of KLF5 transcription factor in cell proliferation and differentiation and its implications for human diseases.Cellular and molecular life sciences : CMLS · 2009Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dimethylnitrosamine administration induces a rapid increase in collagen deposition with concomitant proliferation of hepatic stellate cells in rats. Here, we investigated the pathophysiological profiles of acute and chronic hepatic fibrosis states and attempted to determine the possible role of Kruppel-like factor-5 (KLF5) in this model. In acute study using a single drug injection, we observed a rapid transient increase of ALT and mRNA levels of KLF5 followed by increases in fibrosis-related genes. Repeated administration of dimethylnitrosamine once a week caused early damage with severe fibrosis and sustained hepatocyte injury, while intermittent injections at 2-week intervals induced only modest fibrosis from 3 weeks. Weekly administration also induced profound upregulation of collagen I, alpha-smooth muscle actin, and KLF5 mRNA. In contrast, such continued augmentation was not observed after intermittent injections; KLF5 increased only after 3 weeks. These results suggested that dimethylnitrosamine induced a rapid hepatic fibrogenic response with a possible participation of KLF5.
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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.