Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org
Factor XIII: the cement of the heart after myocardial infarction?
1 Center for Transgene Technology and Gene Therapy and Department of Cardiology, University of Leuven, Belgium
2 Cardiovascular Research Institute Maastricht, Department of Cardiology, P debeyelaan 25, 6202 AZ, Maastricht, The Netherlands
* Corresponding author. Tel: +31 43 3882949, Fax: +31 43 3871055, Email: s.heymans@cardio.unimaas.nl
This editorial refers to Transglutaminase activity in acute infarcts predicts healing outcome and left ventricular remodelling: implications for FXIII therapy and antithrombin use in myocardial infarction by M. Nahrendorf et al.,
on page 445
Footnotes
The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.
| The first 10% of the full text of this article appears below. |
Heart failure (HF) affects >11 million people in the USA and Europe, and ischaemic heart disease accounts for >60% of these patients.1 Despite excellent diagnostic and therapeutic standards for myocardial infarction (MI), improved early phase imaging and therapy are essential to prevent the progression of cardiac dilatation and dysfunction after acute MI.
Transglutaminases (TGs) are a widely distributed group of eight isoenzymes, comprising factor XIII (FXIII) and TG type 1–type 7. They catalyse the post-translational
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EHJ 2008 29: 445-454.[Abstract] [FREE Full Text]