التفاصيل البيبلوغرافية
| العنوان: |
Nicotinamide Riboside Supplementation Restores Myocardial Nicotinamide Adenine Dinucleotide Levels, Improves Survival, and Promotes Protective Environment Post Myocardial Infarction. |
| المؤلفون: |
Tannous, Cynthia, Ghali, Rana, Karoui, Ahmed, Habeichi, Nada J., Amin, Ghadir, Booz, George W., Mericskay, Mathias, Refaat, Marwan, Zouein, Fouad A. |
| المصدر: |
Cardiovascular Drugs & Therapy; Dec2024, Vol. 38 Issue 6, p1385-1396, 12p |
| مستخلص: |
Aims: Myocardial infarction (MI) is a major cause of death. Nicotinamide adenine dinucleotide (NAD+) is a coenzyme in oxidative phosphorylation and substrate of sirtuins and poly-ADP ribose polymerases, enzymes critical for cardiac remodeling post-MI. Decreased NAD+ is reported in several heart failure models with paradoxically an upregulation of nicotinamide riboside kinase 2, which uses nicotinamide riboside (NR) as substrate in an NAD+ biosynthetic pathway. We hypothesized that stimulating nicotinamide riboside kinase 2 pathway by NR supplementation exerts cardioprotective effects. Methods and Results: MI was induced by LAD ligation in 2–3-month-old male mice. NR was administered daily (1 µmole/g body weight) over 7 days. RT-PCR showed a 60-fold increase in nicotinamide riboside kinase 2 expression 4 days post-MI with a 60% drop in myocardial NAD+ and overall survival of 61%. NR restored NAD+ levels and improved survival to 92%. Assessment of respiration in cardiac fibers revealed mitochondrial dysfunction post-MI, and NR improved complexes II and IV activities and citrate synthase activity, a measure of mitochondrial content. Additionally, NR reduced elevated PARP1 levels and activated a type 2 cytokine milieu in the damaged heart, consistent with reduced early inflammatory and pro-fibrotic response. Conclusion: Our data show that nicotinamide riboside could be useful for MI management. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |