Atherosclerosis is a common cardiovascular disease characterised by thickening and stiffening of the arterial wall, loss of elasticity and narrowing of the lumen. The process involves lipid deposition in the arterial intima, inflammatory responses, smooth muscle cell proliferation, and plaque formation.

When arterial plaque ruptures, it triggers thrombosis, leading to acute cardiovascular events, such as myocardial infarction and stroke, which pose a serious threat to human life and health. Therefore, it is of utmost importance to find effective ways to inhibit atherosclerosis and prevent plaque rupture.


1. Improvement of endothelial function

Vascular endothelial cells play a key role in maintaining normal vascular function. Endothelial dysfunction is one of the early events in atherosclerosis.

NMN can improve endothelial function through several pathways. It is a precursor of nicotinamide adenine dinucleotide (NAD +), which activates enzymes related to endothelial cell function, such as SIRT1 (Silent Information Regulator 1).

SIRT1 regulates the activity of endothelial-type nitric oxide synthase (eNOS) and promotes the production of nitric oxide (NO). NO is an important vasodilatory factor, which causes vascular smooth muscle to relax, increases the elasticity of blood vessels, and reduces vasoconstriction and spasms, thereby improving blood flow and inhibiting the development of atherosclerosis.


2. Reducing the inflammatory response

Inflammation plays a central role in the development and progression of atherosclerosis. At the lesion site, inflammatory cells accumulate and release a variety of inflammatory factors that promote lipid deposition and plaque formation.

NMN can attenuate the inflammatory response by modulating inflammation-related signalling pathways. For example, NMN activates SIRT1 by elevating NAD+ levels, which in turn inhibits nuclear factor-κB (NF-κB) activity.

NF - κB is a key inflammatory transcription factor that induces the expression of various inflammatory factors such as interleukin - 6 (IL - 6) and tumour necrosis factor - α (TNF - α). By inhibiting the activity of NF-κB, NMN can reduce the release of inflammatory factors and decrease the infiltration of inflammatory cells, thus slowing down the process of atherosclerosis.


3. Regulation of lipid metabolism

Disorders of lipid metabolism are an important risk factor for atherosclerosis. Excessive low-density lipoprotein (LDL) cholesterol (LDL-C) in the blood is oxidatively modified and then deposited within the arterial walls to form atherosclerotic plaques.

NMN regulates the expression of genes involved in lipid metabolism, lowering the level of LDL-C in the blood while increasing the level of high-density lipoprotein cholesterol (HDL-C).

HDL - C has the function of reverse cholesterol transport, which can transport cholesterol in the artery wall to the liver for metabolism, thus reducing cholesterol deposition in the artery wall.

In addition, NMN can also affect the function of fat cells, reduce the accumulation and release of lipids in fat cells, improve lipid metabolism from the source and prevent atherosclerosis.


4. Stabilising arterial plaque

Preventing arterial plaque rupture is key to preventing acute cardiovascular events.NMN can do this by enhancing plaque stability.

It can regulate the function of smooth muscle cells, allowing them to proliferate and synthesise extracellular matrix within the plaque, increasing the thickness of the plaque's fibrous cap.

At the same time, NMN can inhibit the activity of matrix metalloproteinases (MMPs), a class of enzymes capable of degrading extracellular matrix, whose overactivity leads to a thin, fragile plaque fibrous cap that is prone to rupture. By inhibiting the activity of MMPs, NMN can enhance plaque stability and reduce the risk of plaque rupture.

Although the research on NMN on atherosclerosis is still in progress, the existing research results show its great potential in the prevention and treatment of cardiovascular diseases.