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Updated: Jun 3, 2026
Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
Published on: April 17, 2021
Dietary selenium intake influences Cx43 dephosphorylation, TNF-α expression and cardiac remodeling after reperfused
Stéphane Tanguy1, Andry Rakotovao, Marie-Gabrielle Jouan
1Laboratoire TIMC-IMAG, UMR 5525 CNRS - University of Grenoble, Grenoble, France.
Insights
Dietary selenium intake impacts cardiac remodeling after heart attack. Lower selenium levels worsen heart dysfunction, while adequate selenium may offer cardioprotection by reducing oxidative stress and inflammation.
Area of Science:
- Cardiovascular Science
- Nutritional Biochemistry
- Molecular Cardiology
Background:
- Post-infarct left ventricular dysfunction and cardiac remodeling are leading causes of chronic heart failure.
- Understanding factors influencing cardiac remodeling is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the effect of dietary selenium intake on cardiac remodeling following myocardial infarction.
- To explore the underlying mechanisms of selenium's influence on heart health.
Main Methods:
- Rats were fed diets with either low (0.05 mg/kg) or high (1.50 mg/kg) selenium concentrations.
- Myocardial infarction was induced via transient coronary ligation followed by reperfusion.
- Cardiac remodeling, infarct size, passive compliance, TNF-α, seleno-enzyme activity, and connexin-43 phosphorylation were assessed.
Main Results:
- Low-selenium diet significantly increased infarct size and worsened cardiac remodeling compared to the high-selenium diet.
- Adverse effects in the low-selenium group were associated with elevated cardiac TNF-α and increased connexin-43 dephosphorylation.
- Reduced activity of antioxidant seleno-enzymes was observed in the low-selenium group.
Conclusions:
- Dietary selenium intake significantly influences post-infarct cardiac remodeling.
- Selenium's cardioprotective effects may involve mitigating oxidative stress, reducing TNF-α expression, and modulating connexin-43 dephosphorylation.
Scope:
Post-infarct left ventricular dysfunction and cardiac remodeling are the primary causes of chronic heart failure in industrialized countries. In the present study, we examined the influence of dietary selenium intake on cardiac remodeling after reperfused myocardial infarction and explored one of the possible mechanisms.
Methods And Results:
Rats were fed a diet containing either 0.05 mg/kg (Low-Se, group of rats receiving the low-selenium diet) or 1.50 mg/kg (group of rats receiving the high-selenium diet) selenium. At the end of the 5th week of the diet, rats were subjected to transient (1 h) coronary ligation followed by 8 days of reperfusion. Infarct size and cardiac passive compliance were increased in the Low-Se group compared with group of rats receiving the high-selenium diet. Similarly, indices of cardiac remodeling (thinning index and expansion index) were more altered in Low-Se hearts. These adverse effects of the Low-Se diet on cardiac remodeling were accompanied by an increase in cardiac TNF-α content, a decreased activity of antioxidant seleno-enzymes and an increase in connexin-43 dephosphorylation.
Conclusion:
Dietary selenium intake influences post-infarct cardiac remodeling even when provided within the range of physiological values. Our data suggest that the cardioprotective effect of selenium might be mediated by a reduced oxidative stress, a lower connexin-43 dephosphorylation, and a decreased TNF-α expression.
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