Abstract | BACKGROUND: AIM: To determine whether TK deficiency in the mouse influences survival and cardiac remodelling after MI. METHODS: MI was induced in 10 week-old male TK-deficient mice and wild-type littermates. Survival was assessed up to 14 months. Cardiac morphological and functional parameters were serially measured by echocardiography. In another experiment, myocardial capillary density and NOS content were evaluated at 3 months. RESULTS:
Infarct size was similar in both genotypes. MI resulted in severe cardiac dysfunction. Up to 12 months after MI, TK(-/-) mice displayed an increased mortality rate (P<0.05, relative risk of death=3.41) and aggravation of left ventricular hypertrophy and dilatation by comparison with TK(+/+) (+18% and +27% respectively, both P<0.05). NOS1 and NOS3 were abnormally regulated in the heart of TK(-/-) mice after MI. CONCLUSIONS: TK exerts a protective role in HF in mice. Coronary effects are probably involved. As partial genetic deficiency in TK activity occurs in humans, TK-deficient subjects may be at increased risk of mortality in HF.
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Authors | Sandrine Pons, Violaine Griol-Charhbili, Christophe Heymes, Paul Fornes, Didier Heudes, Albert Hagege, Xavier Loyer, Pierre Meneton, Jean-François Giudicelli, Jane-Lise Samuel, François Alhenc-Gelas, Christine Richer |
Journal | European journal of heart failure
(Eur J Heart Fail)
Vol. 10
Issue 4
Pg. 343-51
(Apr 2008)
ISSN: 1388-9842 [Print] England |
PMID | 18343196
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Kinins
- Nitric Oxide Synthase
- Tissue Kallikreins
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Topics |
- Animals
- Coronary Circulation
(physiology)
- Disease Models, Animal
- Echocardiography
- Kinins
(physiology)
- Male
- Mice
- Mice, Inbred C57BL
- Mice, Mutant Strains
- Myocardial Contraction
(physiology)
- Myocardial Infarction
(pathology, physiopathology)
- Myocardium
(pathology)
- Nitric Oxide Synthase
(metabolism)
- Organ Size
- Stroke Volume
(physiology)
- Survival Rate
- Tissue Kallikreins
(deficiency, physiology)
- Ventricular Remodeling
(physiology)
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