In a groundbreaking study published in Stem Cell Reviews and Reports in 2023, the research team unveiled compelling evidence demonstrating the therapeutic potential of Nicotinamide Mononucleotide (NMN) in ameliorating myocardial infarction and promoting angiogenesis. Furthermore, the study highlighted the cardioprotective attributes of mesenchymal stem cell-derived extracellular vesicles, showcasing their efficacy in the context of acute myocardial infarction. In a meticulously designed rat model of heart disease, NMN emerged as a pivotal factor in enhancing cardiac function, fostering angiogenesis, and minimizing tissue damage through the modulation of hepatocyte-derived vesicles.

Myocardial infarction, a prevalent heart disease, is characterized by myocardial necrosis resulting from acute and persistent ischemia and hypoxia in the coronary arteries. The study delved into several risk factors associated with myocardial infarction, shedding light on contributors such as over-excitement, dietary irrationality, and atherosclerosis. Over-excitement, leading to increased blood flow, may easily precipitate local ischemia in the body, potentially triggering acute myocardial infarction during such periods.

Dietary irrationality, marked by prolonged consumption of greasy, high-sugar foods, elevates blood fat levels, causing an increase in blood viscosity. This heightened risk of an acute myocardial infarction attack is often compounded by the potential development of obesity in affected patients. Atherosclerosis, associated with long-term smoking, high blood pressure, and other factors, negatively impacts the vascular health of the myocardium, potentially contributing to acute myocardial infarction. In addition to these common causes, there are other potential diseases, including diabetes, arrhythmia, and hypertension, that may heighten the risk of myocardial infarction.

Mesenchymal stem cells (MSCs), characterized by pluripotency and possessing the common attributes of stem cells such as self-renewal and multi-directional differentiation abilities, have demonstrated promise in myocardial infarction treatment. Previous animal studies have indicated that supplementing MSCs after myocardial ischemia enables their differentiation into new cardiomyocytes, thereby restoring cardiac function and reducing the infarction area by 12%.

Moreover, the study highlighted NMN's capacity to enhance cellular autophagy by stimulating mitochondrial biosynthesis, providing energy to cells. This mechanism protects the heart from ischaemia-reperfusion injury and reduces the size of myocardial infarction in healthy rats. Motivated by these findings, the researchers sought to verify whether NMN supplementation could indeed exert a protective effect on the heart.

To delve deeper into the synergistic effects of ghr-MSC and NMN, the researchers divided ischemia-reperfusion model rats into four groups: a control group, a ghr-MSC supplementation group, an NMN supplementation group, and a combined ghr-MSC+NMN supplementation group. Remarkably, rats receiving both ghr-MSC and NMN exhibited a remarkable 40% reduction in myocardial infarction—an improvement significantly surpassing that observed in the ghr-MSC supplementation alone group. While NMN supplementation alone demonstrated a commendable 20% reduction in the infarction area in the model rats, the combined effect with ghr-MSC proved to be even more efficacious.


The researchers then delved into the underlying principles behind the heightened effectiveness of the ghr-MSC+NMN combination. It was revealed that NMN supplementation significantly reduced the level of mitochondrial oxidative stress in rat cardiomyocytes. Given that oxidative stress is a pivotal contributor to cardiac injury, the degree of injury was found to be only about half in the presence of NMN, underscoring the profound protective impact of this supplementation. This groundbreaking research not only expands our understanding of NMN's therapeutic potential but also highlights the synergistic benefits achieved when combined with mesenchymal stem cell supplementation in the treatment of myocardial infarction.