NMN can improve NAD+ homeostasis in the heart

Heart health is a hot topic that everyone pays attention to. In recent years, the anti-aging drug NMN has also been targeting heart disease. Since NMN can improve NAD+ homeostasis in the heart and alleviate age-related cardiac pathological and physiological changes, it can effectively improve various types of heart health problems.

In April 2022, the research team of Fudan University Children's Hospital and the School of Life Sciences published a study in JACC (Journal of the American College of Cardiology) stating that NMN can effectively inhibit cardiomyopathy caused by Echs1 deficiency, and published the research results in the journal ScienceDirect superior.

Cardiomyopathy in the elderly is a heterogeneous cardiomyopathy caused by various etiologies including genetic factors, including primary and secondary cardiomyopathy. Cardiomyopathy in the elderly can continue from the young and middle-aged, and some elderly cardiomyopathy is an onset in old age.

Today, the etiology of senile cardiomyopathy is unknown, and there is a lack of specific treatment. Moreover, elderly cardiomyopathy is very complicated, often coexisting with other heart diseases, and it is much more serious than young patients with cardiac insufficiency. The mortality rate of heart failure in the elderly is also higher than that of non-elderly patients, and the mortality rate is related to age. The older the age, the higher the mortality rate. The study found that increasing age, male sex, previous history of myocardial infarction, chronic liver disease, pneumonia, renal failure and cerebral infarction are unfavorable factors affecting the prognosis of elderly patients with heart failure.

Echs1 (short-chain enoyl-CoA hydratase 1) is a key enzyme in fatty acid (FA) and branched-chain amino acid (BCAA) oxidation, which senses nutrient and energy abundance and regulates cell growth and apoptosis. Lack of Echs1 causes cardiac fibrosis in mice.

Echs1 deficiency causes cardiac fibrosis in mice

Echs1 gene-deficient mice were fed a high-NMN diet from the 3rd week to the 8th week, and the left ventricular systolic function was significantly restored at the 8th week. In addition, Echs1 gene-deficient animals significantly reduced cardiac fibrosis after taking NMN.

NMN effectively prevents the development of cardiomyopathy in Echs1 gene-deficient animals

This is because NMN increases Echs1 in the heart, binds to p300 in the cytoplasm, reduces the transfer of p300 to the nucleus, and at the same time controls the acetylation of chromatin H3K9 by stimulating SIRT enzymes, inhibiting myocardial disease caused by the lack of Esch1.

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