ArticleCardiovascular research2017
Tissue transglutaminase induction in the pressure-overloaded myocardium regulates matrix remodelling.
Article in Cardiovascular research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 40 citations in OpenAlex.
- Cardiac fibroblasts in myocardial injury and heart failure.European heart journal · 2026Review
- Role and Mechanism of Lamellar Derived Growth Factor /AKT Pathway in Ventricular Remodeling Induced by Pressure Overload.Cell biochemistry and biophysics · 2025Article
- Pathogenetic Contributions and Therapeutic Implications of Transglutaminase 2 in Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Proteomic profiling of epicardial fat in heart failure with preserved versus reduced and mildly reduced ejection fraction.Journal of cellular and molecular medicine · 2023Article
- Article
- Tissue mechanics coevolves with fibrillar matrisomes in healthy and fibrotic tissues.Matrix biology : journal of the International Society for Matrix Biology · 2022Review
- Fibroblasts orchestrate cellular crosstalk in the heart through the ECM.Nature cardiovascular research · 2022Article
- Right versus left ventricular remodeling in heart failure due to chronic volume overload.Scientific reports · 2021Article
- Cardiac fibrosis.Cardiovascular research · 2021Review
- Collagen denaturation in the infarcted myocardium involves temporally distinct effects of MT1-MMP-dependent proteolysis and mechanical tension.Matrix biology : journal of the International Society for Matrix Biology · 2021Article
- Cross your heart? Collagen cross-links in cardiac health and disease.Cellular signalling · 2021Review
- Sunitinib-induced cardiac hypertrophy and the endothelin axis.Theranostics · 2021Article
- The role of Smad signaling cascades in cardiac fibrosis.Cellular signalling · 2021Review
- The Extracellular Matrix in Ischemic and Nonischemic Heart Failure.Circulation research · 2019Review
- Transglutaminases in Monocytes and Macrophages.Medical sciences (Basel, Switzerland) · 2018Review
- Biocatalysis by Transglutaminases: A Review of Biotechnological Applications.Micromachines · 2018Review
- Cardiac fibrosis can be attenuated by blocking the activity of transglutaminase 2 using a selective small-molecule inhibitor.Cell death & disease · 2018Article
- Pharmacologic inhibition of the enzymatic effects of tissue transglutaminase reduces cardiac fibrosis and attenuates cardiomyocyte hypertrophy following pressure overload.Journal of molecular and cellular cardiology · 2018Article
- Tissue transglutaminase in the pathogenesis of heart failure.Cell death and differentiation · 2018Review
- Left atrial remodeling, hypertrophy, and fibrosis in mouse models of heart failure.Cardiovascular pathology : the official journal of the Society for Cardiovascular PathologyArticle
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
aimsTissue transglutaminase (tTG) is induced in injured and remodelling tissues, and modulates cellular phenotype, while contributing to matrix cross-linking. Our study tested the hypothesis that tTG may be expressed in the pressure-overloaded myocardium, and may regulate cardiac function, myocardial fibrosis and chamber remodelling. METHODS AND
resultsIn order to test the hypothesis, wild-type and tTG null mice were subjected to pressure overload induced through transverse aortic constriction. Moreover, we used isolated cardiac fibroblasts and macrophages to dissect the mechanisms of tTG-mediated actions. tTG expression was upregulated in the pressure-overloaded mouse heart and was localized in cardiomyocytes, interstitial cells, and in the extracellular matrix. In contrast, expression of transglutaminases 1, 3, 4, 5, 6, 7 and FXIII was not induced in the remodelling myocardium. In vitro, transforming growth factor (TGF)-β1 stimulated tTG synthesis in cardiac fibroblasts and in macrophages through distinct signalling pathways. tTG null mice had increased mortality and enhanced ventricular dilation following pressure overload, but were protected from diastolic dysfunction. tTG loss was associated with a hypercellular cardiac interstitium, reduced collagen cross-linking, and with accentuated matrix metalloproteinase (MMP)2 activity in the pressure-overloaded myocardium. In vitro, tTG did not modulate TGF-β-mediated responses in cardiac fibroblasts; however, tTG loss was associated with accentuated proliferative activity. Moreover, when bound to the matrix, recombinant tTG induced synthesis of tissue inhibitor of metalloproteinases (TIMP)-1 through transamidase-independent actions.
conclusionsFollowing pressure overload, endogenous tTG mediates matrix cross-linking, while protecting the remodelling myocardium from dilation by exerting matrix-preserving actions.
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Registered trials
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