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.
The function of NMN to protect the heart has been demonstrated as early as 14 years, and in the following years, research has continued to prove the benefits of NMN on heart health.
In 2014, a study by the New Jersey School of Medicine found that intraperitoneal injection of NMN in mice significantly increased the level of NAD+ in the heart and prevented the reduction of NAD+ during ischemia, thereby protecting the heart from ischemia/reperfusion injury.
In 2017, a study by Case Western Reserve University School of Medicine found that short-term intraperitoneal injection of NMN, the precursor of NAD+, successfully protected mice from heart failure caused by pressure overload.
In 2018, an editorial "Raising NAD in Heart Failure" published by the top international medical journal website Circulation pointed out that self-supplementation of coenzyme I (NAD +) can also reduce cardiac insufficiency in preclinical models of heart failure.
In 2020, a study by the University of Washington in the United States tested the effects of two different mitochondria-targeting drugs SS-31 (a synthetic tetrapeptide) and NMN, and found that NMN completely reversed age-related defects in cardiac systolic function and could Better to rejuvenate an aging heart.
In 2021, a study by West China Hospital of Sichuan University found that intraperitoneal injection of NMN to mice with cardiac fibrosis can effectively increase NAD+ and SIRT1 (an NAD+-dependent deacetylase), thereby reducing cardiac fibrosis in vivo and fibrogenesis in vitro Cell activation.