ArticleThe American journal of pathology2008
Tissue transglutaminase contributes to interstitial renal fibrosis by favoring accumulation of fibrillar collagen through TGF-beta activation and cell infiltration.
Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 153 citations in OpenAlex.
- Trial
- SPECT as a translational non-invasive method to assess occupancy of the tissue transglutaminase-2 by zampilimab in the mouse lung.Respiratory research · 2026Article
- Structure-activity relationships of hydrophobic small molecule irreversible inhibitors of tissue transglutaminase.RSC medicinal chemistry · 2026Article
- A comprehensive approach to elucidating the pathophysiology of kidney fibrosis based on extracellular vesicle proteomics.Frontiers in physiology · 2026Article
- Critical Role for Transglutaminase 2 in Scleroderma Skin Fibrosis and in the Development of Dermal Sclerosis in a Mouse Model of Scleroderma.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Renal and Vascular Effects of the Allosteric Transglutaminase 2 Modulator LDN-27219 in One-Kidney DOCA-Salt Mice.International journal of molecular sciences · 2025Article
- Advances and challenges in kidney fibrosis therapeutics.Nature reviews. Nephrology · 2025Review
- Reduced glomerular and elevated tubulointerstitial transglutaminase pathway and its inhibition in a rat model of renal warm ischemia: implications for feline chronic kidney disease.Frontiers in veterinary science · 2025Article
- Conformational Modulation of Tissue Transglutaminase via Active Site Thiol Alkylating Agents: Size Does Not Matter.Biomolecules · 2024Article
- Article
- Transglutaminase 2 in diabetes mellitus: Unraveling its multifaceted role and therapeutic implications for vascular complications.Theranostics · 2024Review
- RhoA vesicle trafficking-mediated transglutaminase 2 membrane translocation promotes IgA1 mesangial deposition in IgA nephropathy.JCI insight · 2023Article
- Cell-Impermeable Inhibitors Confirm That Intracellular Human Transglutaminase 2 Is Responsible for the Transglutaminase-Associated Cancer Phenotype.International journal of molecular sciences · 2023Article
- Tissue transglutaminase exacerbates renal fibrosis via alternative activation of monocyte-derived macrophages.Cell death & disease · 2023Article
- Novel irreversible peptidic inhibitors of transglutaminase 2.RSC medicinal chemistry · 2023Article
- Tissue mechanics coevolves with fibrillar matrisomes in healthy and fibrotic tissues.Matrix biology : journal of the International Society for Matrix Biology · 2022Review
- Structure-activity relationships of hydrophobic alkyl acrylamides as tissue transglutaminase inhibitors.RSC medicinal chemistry · 2022Article
- Double-Stranded RNA Enhances Matrix Metalloproteinase-1 and -13 Expressions through TLR3-Dependent Activation of Transglutaminase 2 in Dermal Fibroblasts.International journal of molecular sciences · 2022Article
- Role of the vascular endothelial sodium channel activation in the genesis of pathologically increased cardiovascular stiffness.Cardiovascular research · 2022Review
- Urinary levels of pro-fibrotic transglutaminase 2 (TG2) may help predict progression of chronic kidney disease.PloS one · 2022Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Renal fibrosis is defined by the exaggerated accumulation of extracellular matrix proteins. Tissue transglutaminase (TG2) modifies the stability of extracellular matrix proteins and renders the extracellular matrix resistant to degradation. In addition, TG2 also activates transforming growth factor-beta (TGF-beta). We investigated the involvement of TG2 in the development of renal fibrosis using mice with a knockout of the TG2 gene (KO). These mice were studied at baseline and 12 days after unilateral ureteral obstruction, which induced a significant increase in interstitial TG2 expression in wild-type mice (P < 0.001). Interstitial fibrosis was evident in both groups, but total and fibrillar collagen was considerably lower in KO mice as compared with wild-type (P < 0.001). Similarly, mRNA and protein expression of collagen I were significantly lower in KO animals (P < 0.05). A statistically significant reduction in renal inflammation and fewer myofibroblasts were observed in KO mice (P < 0.01). Free active TGF-beta was decreased in KO mice (P < 0.05), although total (active + latent) TFG-beta concentration did not differ between groups. These results show that mice deficient in TG2 are protected against the development of fibrotic lesions in obstructive nephropathy. This protection results from reduced macrophage and myofibroblast infiltration, as well as from a decreased rate of collagen I synthesis because of decreased TGF-beta activation. Our results suggest that inhibition of TG2 may provide a new and important therapeutic target against the progression of renal 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.