NAD+ regulates vascular homeostasis and delays vascular aging

In this delicate and complex system of the human body, blood vessels are like a criss-crossing “river of life”, responsible for transporting nutrients and oxygen to maintain the operation of life. In recent years, scientists have discovered a magical substance – NAD+, which is playing a remarkable role in the field of vascular health.

As the years go by, age-related aging of blood vessels becomes the “dark hand” behind many health problems.

The vitality of blood vessel endothelial cells decreases, the growth ability gradually declines, and new blood vessels are difficult to generate, just like old pipes are difficult to expand and extend, and can not meet the growing needs of the body.

At the same time, cell death occurs frequently, making the wall of the blood vessel weak and elastic, like a wall that has been in disrepair and can collapse at any time.

The advent of NAD+ brought a turnaround. Studies have shown that when NAD+ levels increase, it is like injecting a vigorous vitality into the blood vessels.

It can accurately act on vascular endothelial cells, activate a series of intracellular signaling pathways, promote endothelial cell proliferation and migration, help new blood vessels grow like bamboo shoots, and ensure that every corner of the body can get sufficient blood irrigation.

More importantly, NAD+ acts as a loyal guardian, reducing cell death. It is involved in regulating the survival mechanism of cells, so that blood vessel cells remain vigorous in harsh environments, and effectively prevent damage and aging of blood vessel walls.

With the dual “stunts” of enhancing blood vessel growth ability and reducing cell death, NAD+ successfully blocked the age-related vascular aging process, lit a light for people’s health and longevity, and opened a new chapter of blood vessel rejuvenation.

In order to properly develop therapies to improve vascular health, Professor Csiszar and his research team at the Center for Aging at the University of Oklahoma published an article “Role of endothelial NAD+ deficiency in age-related vascular disease” in Am J Physiol “dysfunction”, elaborated on the effect of declining NAD+ levels on vasodilation function, possibly resulting in increased blood pressure.

In addition to the intrinsic effects of age, cardiovascular risk factors that promote accelerated aging of blood vessels can lead to cellular NAD+ depletion.

Figure 1 NAD+ deficiency induces vascular endothelial dysfunction
Figure 1 NAD+ deficiency induces vascular endothelial dysfunction

NAD+ promotes angiogenesis mechanism

Figure 2 NAD+ promotes angiogenesis through SIRT1
Figure 2 NAD+ promotes angiogenesis through SIRT1

SIRT1 in endothelial cells is a key mediator of the pro-angiogenic signals secreted by muscle cells.

Improving vascular flow in older people patients by increasing NAD+ levels to promote SIRT1-dependent increases in capillary density during cell migration, germination, and angiogenesis can significantly improve tubule structure while preventing vascular breakdown.

NAD+ guards vascular health

1. Inhibit vascular inflammation

FIG. 3 Mechanism of vascular protection activated by NAD+
FIG. 3 Mechanism of vascular protection activated by NAD+

Studies have shown that old age and chronic systemic low-grade inflammation are major drivers of vascular disease.

By supplementing NAD+, chronic low-grade inflammation and protein acetylation can reduced, autophagy can reactivated, and oxidative metabolism in vascular cells can enhanced, which has a good repairing effect on vascular system dysfunction caused by vascular blockage.

2. Protection of mitochondrial function

Figure 4 NAD+ mitigated mitochondrial and damaged ROS production
Figure 4 NAD+ mitigated mitochondrial and damaged ROS production

Microglia-mediated neuroinflammation plays an important role in vascular dementia, and regulating neuroinflammation has become a promising therapeutic target.

The administration of β-nicotinamide adenine dinucleotide protects mitochondria and reduces ROS production in chronic cerebral hypoperfusion (CCH) rats to salvage cognitive deficits and inhibit vascular neuroinflammation.

3. Prevent vascular aging

Figure 5 β-nicotinamide adenine dinucleotide prevents vascular aging
Figure 5 NAD+ prevents vascular aging

In the aging process, the permeability of the blood-brain barrier gradually increases, and the activity of PARP1 enhanced. As one of the consuming enzymes of NAD+, PARP1 will consume NAD+ excessively, resulting in a decrease in the level of NAD+.

By supplementing NAD+ or inhibiting PARP1 activity, the cerebral vascular lesions and blood-brain barrier damage caused by aging can effectively reversed, and it also has a good protective effect on ischemic stroke models.

conclusion

From the cellular level, it is a coenzyme in many key metabolic reactions in the cell, participating in the tricarboxylic acid cycle of energy metabolism, ensuring the continuous and stable energy supply of cells and maintaining the normal operation of cells.

With the increase of age, the body’s NAD+ level naturally declines, mitochondrial function affected, cell energy output sharply reduced, and aging accelerated.

Supplementing NAD+ is equivalent to injecting vitality into cells and rejuvenating senescent cells.

In gene repair, β-nicotinamide adenine dinucleotide provides a substrate for DNA repair enzyme PARP to help repair damaged DNA, reduce the accumulation of gene mutations, reduce the risk of diseases such as cancer, guard genomic stability, and combat the aging process from the root.

Furthermore, β-nicotinamide adenine dinucleotide activates the Sirtuins family of long-lived proteins, which regulate many physiological functions, including inflammation, apoptosis, and autophagy.

They inhibit chronic inflammation and prevent excessive inflammation from eroding the body.

Promote autophagy, remove damaged cell components in time, optimize the intracellular environment, and comprehensively promote the body’s rejuvenation.

There are various ways to supplement NAD+, including taking its precursor substances, such as NMN (nicotinamide mononucleotide), NR (nicotinamide ribose), which can converted into NAD+ in the body.

Although relevant research has broad prospects, clinical applications still being explored and refined, and NAD+ undoubtedly opens up a promising new path for human aging.

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