Jan 03, 2023 / Author: China Glutathione suppliers & NMN manufacturers
Vascular aging is one of the direct causes of body aging. How to keep blood vessels young has become the focus of research in the field of aging inhibition.
Published in the authoritative journal "Signal Transduction and Targeted Therapy", a study co-authored by Xin Hongbo of Nanchang University, Xue Jianxin and Gan Lu of West China Hospital of Sichuan University showed that: CD38 (one of the NAD+ metabolic pathways) leads to intracellular NAD+ (Nicotinamide adenine dinucleotide) level decline is an important reason for the occurrence of age-related cardiovascular and cerebrovascular diseases, while supplementing NMN (β-Nicotinamide Mononucleotide) or inhibiting CD38 can increase NAD+ levels and delay the development of mice. Vascular smooth muscle cells age and undergo pathological structural changes.
NMN supplementation increases NAD+ levels and alleviates hypertension and vascular structural changes
CD38 can not only decompose NAD+, but also consume NMN and other precursor substances necessary for the synthesis of NAD+. The study found that CD38 gene-deficient mice had nearly 50 percent more intracellular NAD+ levels in the aorta compared with normal mice.
To explore whether NAD+ supplementation can rescue vascular smooth muscle cell aging, the researchers orally administered NMN (300mg/kg) to normal mice. The results showed that NAD+ levels were increased in mice, and the symptoms of angiotensin II-induced hypertension were improved. (See Figure 1.) In addition, the medial thickness, media-to-lumen ratio, and collagen deposition of vessels were reduced by 26%, 27%, and 30%, respectively.
The researchers found that NAD+ is generally involved in the signaling pathways of cardiovascular diseases and can have a repairing effect on cardiovascular diseases by regulating metabolism, maintaining redox homeostasis and regulating immune responses.
At the same time, the intake of NAD+ supplements such as NMN can also delay aging through a variety of molecular pathways, and then intervene in the occurrence and exacerbation of cardiovascular disease, a typical aging-related disease.
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