Unveiling the Modulation of NMN Supplementation on Mitochondrial Homeostasis

Unveiling the Modulation of NMN Supplementation on Mitochondrial Homeostasis



1.Introduction

Mitochondria, a type of highly plastic organelle, can maintain a relatively stable dynamic equilibrium state towards the morphology, structure, quantity, volume, quality, and function under normal physiological conditions. This dynamic equilibrium state is generally called mitochondria homeostasis. Replenishment of nicotinamide mononucleotide (NMN) to boost intracellular NAD+ level can regulate mitochondrial homeostasis.

2.The amelioration of mitochondrial dysfunction and senescence post NMN treatment

Typically, NAD+ level determines the rate and extent of senescence. The NAD+ pool experienced by cells and tissues presents a declined tendency with age, which may lead to a loss of mitochondrial homeostasis and senescent phenotypes in CD8+ T cells. 

Following NMN (100 μM) supplementation, NAD+ level is restored and the NAD+/NADH ratio is elevated in senescent CD8+ T cells, by which the mitochondrial functions are obviously improved and the cytoplasmic mtDNA is reduced.

3.The prevention of neuroinflammation and senescence in CD8+ T cells via NMN supplement

Post NMN supplementation, the senescence and neuroinflammation are correspondingly repressed. With a great detail, NMN supplementation decreases the ROS and mitochondrial membrane potential in CD8+ T cells, while increasing the intracellular ATP. Furthermore, NMN suppresses the inflammation-associated markers (IL-1β, IL-6, TNF-α and IFN-γ) in the supernatant and the mRNA of senescent CD8+ T cells. 

4. The inhibitory effect of NMN on the senescence-related pathway STING

The activation of STING can launch a robust proinflammatory response and senescence, which is closely related to the deficient health span in model mice. Strikingly, NMN can prominently improve the senescent state of T cells and reduce the secretion of senescence-related inflammatory factors via inhibition of the STING pathway.

5. Conclusion

Upregulation of NAD+ level by NMN supplementation can regulate the mitochondrial homeostasis to prevent STING-induced senescence in CD8+ T cells.

Reference

Ye B, Pei Y, Wang L, et al. NAD+ supplementation prevents STING-induced senescence in CD8+ T cells by improving mitochondrial homeostasis. J Cell Biochem. 2024;1-17. doi:10.1002/jcb.30522

BONTAC NMN



BONTAC is the pioneer of NMN industry and the first manufacturer to launch NMN mass production, with the first whole-enzyme catalysis technology around the world. At present, BONTAC has become the leading enterprise in niche areas of coenzyme products. Notably, BONTAC is the NMN raw material supplier of famous David Sinclair team at the Harvard University, who uses the raw materials of BONTAC in a paper titled “Impairment of an Endothelial NAD+-H2S Signaling Network Is a Reversible Cause of Vascular Aging”. Our services and products have been highly recognized by global partners. Furthermore, BONTAC has the first national and the only provincial independent coenzyme engineering technology research center in Guangdong, China. The coenzyme products of BOMNTAC are widely used in fields such as nutritional health, biomedicine, medical beauty, daily chemicals and green agriculture.

Disclaimer

This article is based on the reference in the academic journal. The relevant information is provide for sharing and learning purposes only, and does not represent any medical advice purposes. If there is any infringement, please contact the author for deletion. The views expressed in this article do not represent the position of BONTAC. 

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