Heart Failure? NMN can help reduce the risk of it happening.
In mice deficient in a molecule that makes them prone to heart disease, researchers discovered that NMN administration improved mitochondrial health and prevented heart failure.
In 2017, researchers from Case Western Reserve University, who reported their work in the Journal of Molecular and Cellular Cardiology, discovered that nicotinamide mononucleotide (NMN) supplementation promotes mitochondrial health and protects against heart failure.
Research has discovered that there is a relationship between mitochondrial dysfunction and heart failure. Also, when individuals have reductions in nicotinamide adenine dinucleotide (NAD+), it leads to mitochondrial issues.
NAD+ Role For Heart Failure Prevention
NAD+ is a critical molecule for metabolism and mitochondrial health, yet NAD+ levels in the body decline with age. NAD+ levels are important for protein activity in the body, particularly sirtuins. These proteins remove molecular tags from other proteins in the cell so they can function properly to maintain mitochondrial health.
In their research, the researchers used mice with a deficiency in KLF4, a molecule that controls mitochondrial health. Due to their defective mitochondria, KLF4-deficient mice are more susceptible to heart pressure overload-induced heart failure. The cellular mechanisms behind these effects were unknown, and the team of researchers wanted to know why.
In the study, researchers discovered that KLF4-deficient mice had considerably higher amounts of molecular tags on their mitochondrial proteins, which sirtuins, in particular Sirt3, should remove. The scientists found lower levels of Sirt3 and NAD+ in the hearts of rats with heart health problems.
High NAD+ levels might limit the activity of Sirt3, which is dependent on NAD+. Higher levels of molecular tags on mitochondrial proteins may impair mitochondrial health by limiting the function of NAD+-dependent Sirt3.
Raise NAD+ Levels
By injecting the animals with NMN, a molecule that boosts NAD+, the levels of NAD+ content in the mice increased. After the administration of NMN, KLF4-deficient mice had less activated inflammation genes.
Several studies have shown that overactive inflammation genes play a role in heart disease. Mice treated with NMN had normal cardiac responses to induced blood pressure overload, as well as reduced expression of inflammation genes.
In mice lacking KLF4, a protein important for heart health, there is a high mortality rate. However, after being given NMN - a nicotinamide mononucleotide that occurs naturally in the body - 100% of these same mice survived despite having high blood pressure induced in their hearts. These results show that NMN can prevent heart failure even in those animals most sensitive to developing this condition.
Prevention Of Heart Failure
Not only does the prevention of heart failure correlate with mitochondrial health, but also KLF4-deficient mice. These miuse have degenerated and fragmentd mitochondria; however, NMN treatments almost completely restore the structure.
“Short-term administration of NMN, a precursor of NAD+, preserved mitochondrial homeostasis and rescued heart function from pressure overload-induced heart failure,” stated the scientists of the study.
NMN was linked to improved mitochondrial function and cardiac survival in several animal studies, according to researchers at Northwestern University Feinberg School of Medicine. It was also shown to increase NAD+ levels and improve sirtuin activity.
Treatment with NMN enhances the function of sirtuins, which leads to a decrease in molecular tagging and an improvement in the activation of proteins in mitochondria important for cell energy production and health. Following these results, NMN may be used to treat heart failure.