ArticleGastroenterology2011
Tissue transglutaminase does not affect fibrotic matrix stability or regression of liver fibrosis in mice.
Article in Gastroenterology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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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.
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Who cites it
78 citing papers in PubMed, 140 citations in OpenAlex.
- The Matrix Reloaded: The Hepatic Matrisome as a Therapeutic Opportunity to Fight Liver Fibrosis.Biomolecules · 2026Review
- Upcoming Treatments in Celiac Disease: From Luminal Enzymes to Oral Immune Tolerance.United European gastroenterology journal · 2026Review
- A novel cell-permeable LOXL2 inhibitor PAT-1251 potently suppresses biliary liver fibrosis via collagen crosslinking-dependent and -independent mechanisms.Hepatology communications · 2026Article
- Stiffness-activated hepatic stellate cells boost HCC migration via TGM2/ITGB1-mediated matrix remodeling and mitochondrial transfer.JHEP reports : innovation in hepatology · 2025Article
- Myeloperoxidase, extracellular DNA and neutrophil extracellular trap formation in the animal models of metabolic dysfunction-associated steatotic liver disease.World journal of gastroenterology · 2025Article
- Role of transglutaminase 2 in promoting biglycan synthesis in idiopathic gingival fibromatosis.BMC oral health · 2024Article
- Mi-BMSCs alleviate inflammation and fibrosis in CClMaterials today. Bio · 2024Article
- Crosstalk of lysyl oxidase-like 1 and lysyl oxidase prolongs their half-lives and regulates liver fibrosis through Notch signal.Hepatology communications · 2024Article
- CA19-9-related macrophage polarization drives poor prognosis in HCC after immune checkpoint inhibitor treatment.Frontiers in oncology · 2024Article
- Beneficial Effects of a Curcumin Derivative and Transforming Growth Factor-β Receptor I Inhibitor Combination on Nonalcoholic Steatohepatitis.Diabetes & metabolism journal · 2023Article
- Article
- Regulatory T-cell deficiency leads to features of autoimmune liver disease overlap syndrome in scurfy mice.Frontiers in immunology · 2023Article
- Increased CHCHD2 expression promotes liver fibrosis in nonalcoholic steatohepatitis via Notch/osteopontin signaling.JCI insight · 2022Article
- Automated whole slide image analysis for a translational quantification of liver fibrosis.Scientific reports · 2022Article
- Tissue mechanics coevolves with fibrillar matrisomes in healthy and fibrotic tissues.Matrix biology : journal of the International Society for Matrix Biology · 2022Review
- The prophylactic and anti-fibrotic activity of phthalimido-thiazole derivatives in schistosomiasis mansoni.Parasitology research · 2022Article
- Article
- Air pollution particles hijack peroxidasin to disrupt immunosurveillance and promote lung cancer.eLife · 2022Article
- Ruxolitinib suppresses liver fibrosis progression and accelerates fibrosis reversal via selectively targeting Janus kinase 1/2.Journal of translational medicine · 2022Article
- Therapeutic potential of macrophage colony-stimulating factor in chronic liver disease.Disease models & mechanisms · 2022Article
18 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsThe ubiquitous cross-linking enzyme tissue transglutaminase (TG2) has been implicated in irreversible collagen stabilization in liver fibrosis, although functional evidence is lacking. We studied the contribution of TG2 to hepatic fibrotic matrix stability, as well as liver fibrosis progression and regression in TG2-deficient mice.
methodsAdvanced liver fibrosis was induced by carbon tetrachloride or thioacetamide in TG2(-/-) mice and their wild-type littermates to study fibrosis progression and its spontaneous regression for up to 36 weeks. Pattern and extent of fibrosis were analyzed by histology and hepatic hydroxyproline quantification. Dynamic changes in hepatic matrix cross-linking were assessed by stepwise collagen extraction. Expression of 7 TGs and fibrosis-related genes was determined by quantitative reverse-transcription polymerase chain reaction.
resultsTransglutaminase activity was increased in fibrosis, and the level of TG2 messenger RNA correlated with the expression of fibrosis-related genes. Biochemical analysis revealed progressive collagen stabilization, with an up to 6-fold increase in the highly cross-linked, pepsin-insoluble fraction (26%). In TG2(-/-) mice, hepatic TG activity was significantly decreased, but chronic administration of carbon tetrachloride or thioacetamide led to a comparable extent and pattern of liver fibrosis, as in wild-type mice. In TG2(-/-) mice, the composition of hepatic collagen fractions and levels of fibrosis-related transcripts were unchanged, and fibrosis reversal was not facilitated.
conclusionsTG2 and TG activity are up-regulated during hepatic fibrosis progression, but do not contribute to fibrogenesis or stabilization of the collagen matrix. TG2 deletion does not promote regression of liver fibrosis. TG2-independent collagen cross-linking is a remarkable feature of progressing hepatic fibrosis and represents an important therapeutic target for liver fibrosis.
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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.