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Peer-reviewedCC BY 4.0Cell Death Discovery

Transglutaminase 2 contributes to the blood clotting cascade

  • Mauro Piacentini1
  • Nicola J. Mutch2
  • Alessandro Mauriello1
  • Manuel Scimeca1
  • Mara Mancini1
  • Valerio Da Ros3
  • Francesco Barilla’1
  • Yufang Shi4
  • Eleonora Candi1,5
  • Zhuo Wang6
  • Martin Griffin6
  • Gerry Melino1
6 affiliations
  1. 1Department of Experimental Medicine, University of Rome “Tor Vergata”, Rome, Italy
  2. 2Aberdeen Diabetes and Cardiovascular Centre, Institute of Medical Sciences, School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Aberdeen, UK
  3. 3Department of Biomedicine and Prevention, University Hospital of Rome “Tor Vergata”, Rome, Italy
  4. 4The Fourth Affiliated Hospital of Soochow University, Institutes for Translational Medicine, Suzhou Medical College, Soochow University, Suzhou, China
  5. 5Fondazione Luigi Maria Monti IDI-IRCCS, Rome, Italy
  6. 6Department of Biosciences, School of Health and Life Sciences, Aston Triangle, Aston University, Birmingham, UK
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Abstract

Cross-linking of fibrin and associated proteins via Nε-(γ-glutamyl)lysine bonds in clot formation is a well-established component of the hemodynamic mechanism, providing clot rigidity and reducing the rate of fibrinolysis. The latter effect occurs predominantly through the incorporation of fibrinolytic inhibitors. To date, this function has been attributed exclusively to Factor XIIIa, also known as plasma transglutaminase (TG), one of eight identified in mammals. In this report, we demonstrate that tissue transglutaminase (TG2), a ubiquitous enzyme abundantly present in erythrocytes, also contributed to clot stabilisation. We observed clear differences between whole thrombi isolated from TG2-deficient and wild-type mice. Similarly, human thrombi were more stable in the presence of TG2 than when TG2 activity is specifically inhibited, revealing a previously unrecognized role for this enzyme in haemostasis. Therefore, we propose TG2 as an additional factor involved in blood coagulation.

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Cite

BibTeXRIS
BibTeX
@article{piacentini2026transglutaminase,
  title = {{Transglutaminase 2 contributes to the blood clotting cascade}},
  author = {Mauro Piacentini and Nicola J. Mutch and Alessandro Mauriello and Manuel Scimeca and Mara Mancini and Valerio Da Ros and Francesco Barilla’ and Yufang Shi and Eleonora Candi and Zhuo Wang and Martin Griffin and Gerry Melino},
  journal = {Cell Death Discovery},
  year = {2026},
  month = oct,
  doi = {10.1038/s41420-026-03388-1},
  url = {https://doi.org/10.1038/s41420-026-03388-1},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Transglutaminase 2 contributes to the blood clotting cascade
AU  - Mauro Piacentini
AU  - Nicola J. Mutch
AU  - Alessandro Mauriello
AU  - Manuel Scimeca
AU  - Mara Mancini
AU  - Valerio Da Ros
AU  - Francesco Barilla’
AU  - Yufang Shi
AU  - Eleonora Candi
AU  - Zhuo Wang
AU  - Martin Griffin
AU  - Gerry Melino
PY  - 2026
DA  - 2026/10/17
JO  - Cell Death Discovery
DO  - 10.1038/s41420-026-03388-1
UR  - https://doi.org/10.1038/s41420-026-03388-1
AB  - Cross-linking of fibrin and associated proteins via Nε-(γ-glutamyl)lysine bonds in clot formation is a well-established component of the hemodynamic mechanism, providing clot rigidity and reducing the rate of fibrinolysis. The latter effect occurs predominantly through the incorporation of fibrinolytic inhibitors. To date, this function has been attributed exclusively to Factor XIIIa, also known as plasma transglutaminase (TG), one of eight identified in mammals. In this report, we demonstrate that tissue transglutaminase (TG2), a ubiquitous enzyme abundantly present in erythrocytes, also contributed to clot stabilisation. We observed clear differences between whole thrombi isolated from TG2-deficient and wild-type mice. Similarly, human thrombi were more stable in the presence of TG2 than when TG2 activity is specifically inhibited, revealing a previously unrecognized role for this enzyme in haemostasis. Therefore, we propose TG2 as an additional factor involved in blood coagulation.
SN  - 2058-7716
ER  -