AI Article Synopsis
- Myocardial infarction (MI) is a complex heart condition arising from various genetic and environmental influences, linked to coronary artery disease.
- There is growing evidence that Nicotinamide Adenine Dinucleotide (NAD) plays a critical role in metabolic regulation and may serve as a potential treatment for MI.
- This review focuses on how NAD signaling affects sirtuin (SIRT) deacetylase activity and its implications for improving MI treatment outcomes.
Article Abstract
Myocardial infarction (MI) is one of the complex phenotypes of coronary artery disease, which results from the interaction of multiple genetic and environmental factors. Nicotinamide Adenine Dinucleotide (NAD) is an important cofactor regulating metabolic homeostasis and a rate-limiting substrate for sirtuin (SIRT) deacetylase. Numerous NAD studies have shown that it can be used as an anti-MI treatment. However, there have been few systematic reviews of the overall role of NAD in treating MI. MI, which has long been a global health problem, still lacks effective treatment till now, and the discovery of NAD provides a new perspective on its adjuvant treatment. This review summarizes the role of NAD signaling in SIRTs in alleviating MI.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10663897 | PMC |
| http://dx.doi.org/10.1016/j.heliyon.2023.e21890 | DOI Listing |
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